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Gene Information
Gene symbol: PTGS2
Gene name: prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)
HGNC ID: 9605
Synonyms: COX2
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 11982590 | BCG stimulated thioglycollate-elicited murine peritoneal exudate cells (PEC) to induce cytotoxic activity and to produce cytokines such as interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha and PGE2. |
| 2 | 11982590 | NS398, a specific COX-2 inhibitor, and indomethacin (IM), a COX-1 and COX-2 inhibitor, enhanced viable BCG-induced cytotoxic activity and IFN-gamma and TNF-alpha production of PEC. |
| 3 | 11982590 | Enhanced cytotoxicity was mediated by increased amounts of IFN-gamma and TNF-alpha. |
| 4 | 11982590 | Exogenous PGE2 reduced cytotoxic activity and IFN-gamma and TNF-alpha production of PEC. |
| 5 | 12047757 | Macrophages showed a rapid inflammatory response in which the expression of interleukin-1beta (IL-1beta), major histocompatibility complex class II (MHC II), inducible cyclo-oxygenase (Cox-2), and inducible nitric oxide synthase (iNOS) was enhanced, but tumour necrosis factor-alpha (TNF-alpha) expression was greatly reduced initially and then increased. |
| 6 | 12047757 | After 5 days, except for TNF-alpha and MHC II, expression returned to levels approaching those of uninfected macrophages. |
| 7 | 12047757 | We found that msa reduced the expression of IL-1beta, Cox-2, and MHC II but stimulated TNF-alpha while hly, rsh and grp stimulated MHC II but down-regulated TNF-alpha. |
| 8 | 12047757 | Constructs expressing hly or lysB stimulated iNOS expression and additionally, lysB stimulated TNF-alpha. |
| 9 | 12047757 | The results show how p57 suppresses the host immune system and suggest that the immune mechanisms for the containment of R. salmoninarum infections rely on MHC II- and TNF-alpha-dependent pathways. |
| 10 | 12047757 | Macrophages showed a rapid inflammatory response in which the expression of interleukin-1beta (IL-1beta), major histocompatibility complex class II (MHC II), inducible cyclo-oxygenase (Cox-2), and inducible nitric oxide synthase (iNOS) was enhanced, but tumour necrosis factor-alpha (TNF-alpha) expression was greatly reduced initially and then increased. |
| 11 | 12047757 | After 5 days, except for TNF-alpha and MHC II, expression returned to levels approaching those of uninfected macrophages. |
| 12 | 12047757 | We found that msa reduced the expression of IL-1beta, Cox-2, and MHC II but stimulated TNF-alpha while hly, rsh and grp stimulated MHC II but down-regulated TNF-alpha. |
| 13 | 12047757 | Constructs expressing hly or lysB stimulated iNOS expression and additionally, lysB stimulated TNF-alpha. |
| 14 | 12047757 | The results show how p57 suppresses the host immune system and suggest that the immune mechanisms for the containment of R. salmoninarum infections rely on MHC II- and TNF-alpha-dependent pathways. |
| 15 | 12949405 | Cyclooxygenase (COX) enzymes catalyze the synthesis of prostaglandins and exist as two isoforms, COX-1 and COX-2. |
| 16 | 14747048 | Current novel approaches include vaccines, cyclooxygenase-2 (COX-2) inhibitors, selective apoptotic antineoplastic drugs, endothelin-A receptor antagonists, chemotherapy, vitamin D, and peroxisome proliferator-activated receptor-gamma agonists. |
| 17 | 14747048 | These therapies, such as the COX-2 inhibitors, will need to proceed to phase 3 trials to answer the more important question of whether this change in PSA dynamics translates into improved survival. |
| 18 | 14747048 | Current novel approaches include vaccines, cyclooxygenase-2 (COX-2) inhibitors, selective apoptotic antineoplastic drugs, endothelin-A receptor antagonists, chemotherapy, vitamin D, and peroxisome proliferator-activated receptor-gamma agonists. |
| 19 | 14747048 | These therapies, such as the COX-2 inhibitors, will need to proceed to phase 3 trials to answer the more important question of whether this change in PSA dynamics translates into improved survival. |
| 20 | 15150127 | The present study was designed to determine whether: (a) chronic administration of dietary celecoxib (Celebrex), a potent nonsteroidal anti-inflammatory drug, which targets the cyclooxygenase-2 (COX-2) enzyme, negatively impacts host immunity; and (b) celecoxib can be coupled with a poxvirus-based vaccine to impact tumor burden in a murine tumor model of spontaneous adenomatous polyposis coli. |
| 21 | 15150127 | Responses of splenic T, B, and natural killer cells to broad-based and antigen-specific stimuli were, for the most part, unchanged in those mice as well as COX-2 knockout mice; exceptions included: (a) reduced IFN-gamma production by concanavalin A- or antigen-stimulated T cells; and (b) heightened lipopolysaccharide response of naive B cells from mice fed a diet supplemented with 1000 ppm of celecoxib. |
| 22 | 15150127 | When transgenic mice that express the human carcinoembryonic antigen (CEA) gene (CEA transgenic) were bred with mice bearing a mutation in the Apc(Delta850) gene (multiple intestinal neoplasia mice), the progeny (CEA transgenic/multiple intestinal neoplasia) spontaneously develop multiple intestinal neoplasms that overexpress CEA and COX-2. |
| 23 | 15150127 | The present study was designed to determine whether: (a) chronic administration of dietary celecoxib (Celebrex), a potent nonsteroidal anti-inflammatory drug, which targets the cyclooxygenase-2 (COX-2) enzyme, negatively impacts host immunity; and (b) celecoxib can be coupled with a poxvirus-based vaccine to impact tumor burden in a murine tumor model of spontaneous adenomatous polyposis coli. |
| 24 | 15150127 | Responses of splenic T, B, and natural killer cells to broad-based and antigen-specific stimuli were, for the most part, unchanged in those mice as well as COX-2 knockout mice; exceptions included: (a) reduced IFN-gamma production by concanavalin A- or antigen-stimulated T cells; and (b) heightened lipopolysaccharide response of naive B cells from mice fed a diet supplemented with 1000 ppm of celecoxib. |
| 25 | 15150127 | When transgenic mice that express the human carcinoembryonic antigen (CEA) gene (CEA transgenic) were bred with mice bearing a mutation in the Apc(Delta850) gene (multiple intestinal neoplasia mice), the progeny (CEA transgenic/multiple intestinal neoplasia) spontaneously develop multiple intestinal neoplasms that overexpress CEA and COX-2. |
| 26 | 15150127 | The present study was designed to determine whether: (a) chronic administration of dietary celecoxib (Celebrex), a potent nonsteroidal anti-inflammatory drug, which targets the cyclooxygenase-2 (COX-2) enzyme, negatively impacts host immunity; and (b) celecoxib can be coupled with a poxvirus-based vaccine to impact tumor burden in a murine tumor model of spontaneous adenomatous polyposis coli. |
| 27 | 15150127 | Responses of splenic T, B, and natural killer cells to broad-based and antigen-specific stimuli were, for the most part, unchanged in those mice as well as COX-2 knockout mice; exceptions included: (a) reduced IFN-gamma production by concanavalin A- or antigen-stimulated T cells; and (b) heightened lipopolysaccharide response of naive B cells from mice fed a diet supplemented with 1000 ppm of celecoxib. |
| 28 | 15150127 | When transgenic mice that express the human carcinoembryonic antigen (CEA) gene (CEA transgenic) were bred with mice bearing a mutation in the Apc(Delta850) gene (multiple intestinal neoplasia mice), the progeny (CEA transgenic/multiple intestinal neoplasia) spontaneously develop multiple intestinal neoplasms that overexpress CEA and COX-2. |
| 29 | 15271932 | This strategy identified five antigens, four of which were previously reported (ALT-2, TPX-2, VAH and COX-2) and the other one was a novel cuticular collagen (Col-4). |
| 30 | 16002678 | Treatment of naive mice with the COX-2 inhibitor, SC-58236, skewed splenocytes toward a type 1 cytokine response, inducing IFN-gamma, IL-12, and IFN-gamma-inducible protein 10, whereas the type 2 cytokines IL-4, IL-5, and IL-10 remained unaltered. |
| 31 | 16002678 | Studies performed in CD4 and CD8 knockout mice revealed a requirement for the CD4 T lymphocyte subset for the complete rejection of tumors. |
| 32 | 16002678 | In vivo depletion of IFN-gamma abrogated the COX-2 inhibitor-mediated enhancement of the vaccination effect. |
| 33 | 16002678 | Treatment of naive mice with the COX-2 inhibitor, SC-58236, skewed splenocytes toward a type 1 cytokine response, inducing IFN-gamma, IL-12, and IFN-gamma-inducible protein 10, whereas the type 2 cytokines IL-4, IL-5, and IL-10 remained unaltered. |
| 34 | 16002678 | Studies performed in CD4 and CD8 knockout mice revealed a requirement for the CD4 T lymphocyte subset for the complete rejection of tumors. |
| 35 | 16002678 | In vivo depletion of IFN-gamma abrogated the COX-2 inhibitor-mediated enhancement of the vaccination effect. |
| 36 | 16204627 | Splenic PGE2-M Ø from Balb/c mice, given 0.01 or 1 mg heat-killed (HK) Mycobacterium bovis bacillus Calmette-Guerin (BCG) intraperitoneally (i.p.), were characterized by the ex vivo release of PGE2 (>10 ng/10(6) cells), cytokine production, and expression of PGG/H synthase (PGHS)-1, PGHS-2, cytosolic PGE synthase (PGES), and microsomal PGES-1. |
| 37 | 16204627 | At Day 14 after the treatment, mice treated with 1 mg, but not 0.01 mg, BCG had increased levels of PGHS-2+ PGE2-MØ, total serum immunoglobulin E (IgE), and serum IgG1 antibodies (Th2 responses) against heat shock protein 65 and purified protein derivative. |
| 38 | 16204627 | Cultures of spleen cells isolated from these mice expressed interleukin (IL)-4 and IL-10 in recall responses. |
| 39 | 16204627 | Treatment of mice receiving 1 mg BCG with NS-398 (a PGHS-2 inhibitor, 10 mg/kg i.p., daily) resulted in enhanced interferon-gamma (IFN-gamma) production with reduced IL-4 and IL-10 production in recall responses. |
| 40 | 16204627 | Treatment of C57Bl/6 mice with HK-BCG (0.5 mg dose) also induced a mixture of Th1 and Th2 responses, although IFN-gamma production was markedly increased, and IL-4 was decreased compared with Balb/c mice. |
| 41 | 16204627 | Splenic PGE2-M Ø from Balb/c mice, given 0.01 or 1 mg heat-killed (HK) Mycobacterium bovis bacillus Calmette-Guerin (BCG) intraperitoneally (i.p.), were characterized by the ex vivo release of PGE2 (>10 ng/10(6) cells), cytokine production, and expression of PGG/H synthase (PGHS)-1, PGHS-2, cytosolic PGE synthase (PGES), and microsomal PGES-1. |
| 42 | 16204627 | At Day 14 after the treatment, mice treated with 1 mg, but not 0.01 mg, BCG had increased levels of PGHS-2+ PGE2-MØ, total serum immunoglobulin E (IgE), and serum IgG1 antibodies (Th2 responses) against heat shock protein 65 and purified protein derivative. |
| 43 | 16204627 | Cultures of spleen cells isolated from these mice expressed interleukin (IL)-4 and IL-10 in recall responses. |
| 44 | 16204627 | Treatment of mice receiving 1 mg BCG with NS-398 (a PGHS-2 inhibitor, 10 mg/kg i.p., daily) resulted in enhanced interferon-gamma (IFN-gamma) production with reduced IL-4 and IL-10 production in recall responses. |
| 45 | 16204627 | Treatment of C57Bl/6 mice with HK-BCG (0.5 mg dose) also induced a mixture of Th1 and Th2 responses, although IFN-gamma production was markedly increased, and IL-4 was decreased compared with Balb/c mice. |
| 46 | 16204627 | Splenic PGE2-M Ø from Balb/c mice, given 0.01 or 1 mg heat-killed (HK) Mycobacterium bovis bacillus Calmette-Guerin (BCG) intraperitoneally (i.p.), were characterized by the ex vivo release of PGE2 (>10 ng/10(6) cells), cytokine production, and expression of PGG/H synthase (PGHS)-1, PGHS-2, cytosolic PGE synthase (PGES), and microsomal PGES-1. |
| 47 | 16204627 | At Day 14 after the treatment, mice treated with 1 mg, but not 0.01 mg, BCG had increased levels of PGHS-2+ PGE2-MØ, total serum immunoglobulin E (IgE), and serum IgG1 antibodies (Th2 responses) against heat shock protein 65 and purified protein derivative. |
| 48 | 16204627 | Cultures of spleen cells isolated from these mice expressed interleukin (IL)-4 and IL-10 in recall responses. |
| 49 | 16204627 | Treatment of mice receiving 1 mg BCG with NS-398 (a PGHS-2 inhibitor, 10 mg/kg i.p., daily) resulted in enhanced interferon-gamma (IFN-gamma) production with reduced IL-4 and IL-10 production in recall responses. |
| 50 | 16204627 | Treatment of C57Bl/6 mice with HK-BCG (0.5 mg dose) also induced a mixture of Th1 and Th2 responses, although IFN-gamma production was markedly increased, and IL-4 was decreased compared with Balb/c mice. |
| 51 | 16269200 | Upon exposure to the various MS types, Mphi increased only the production of reactive oxygen intermediates (ROI), while the production of nitric oxide (NO), tumor necrosis factor alpha (TNF-alpha), and the expression of cyclooxigenase-2 (COX-2), inducible NO synthase (iNOS), the cell surface markers MHC class I and II, and CD 86 remained unaffected. |
| 52 | 16272346 | Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection. |
| 53 | 16272346 | The cyclooxygenase (COX) pathway is important in modulating immune responses and is also a major target of nonsteroidal anti-inflammatory drugs (NSAIDs) and the newer COX-2 inhibitors. |
| 54 | 16272346 | The purpose of the present study was to examine the effect of deficiency of COX-1 or COX-2 on the host response to influenza. |
| 55 | 16272346 | We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice. |
| 56 | 16272346 | Infection induced less severe illness in COX-2-/- mice in comparison to WT and COX-1-/- mice as evidenced by body weight and body temperature changes. |
| 57 | 16272346 | COX-1-/- mice had enhanced inflammation and earlier appearance of proinflammatory cytokines in the BAL fluid, whereas the inflammatory and cytokine responses were blunted in COX-2-/- mice. |
| 58 | 16272346 | However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection. |
| 59 | 16272346 | Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection. |
| 60 | 16272346 | Thus, deficiency of COX-1 and COX-2 leads to contrasting effects in the host response to influenza infection, and these differences are associated with altered production of prostaglandins and leukotrienes following infection. |
| 61 | 16272346 | COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection. |
| 62 | 16272346 | Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection. |
| 63 | 16272346 | The cyclooxygenase (COX) pathway is important in modulating immune responses and is also a major target of nonsteroidal anti-inflammatory drugs (NSAIDs) and the newer COX-2 inhibitors. |
| 64 | 16272346 | The purpose of the present study was to examine the effect of deficiency of COX-1 or COX-2 on the host response to influenza. |
| 65 | 16272346 | We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice. |
| 66 | 16272346 | Infection induced less severe illness in COX-2-/- mice in comparison to WT and COX-1-/- mice as evidenced by body weight and body temperature changes. |
| 67 | 16272346 | COX-1-/- mice had enhanced inflammation and earlier appearance of proinflammatory cytokines in the BAL fluid, whereas the inflammatory and cytokine responses were blunted in COX-2-/- mice. |
| 68 | 16272346 | However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection. |
| 69 | 16272346 | Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection. |
| 70 | 16272346 | Thus, deficiency of COX-1 and COX-2 leads to contrasting effects in the host response to influenza infection, and these differences are associated with altered production of prostaglandins and leukotrienes following infection. |
| 71 | 16272346 | COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection. |
| 72 | 16272346 | Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection. |
| 73 | 16272346 | The cyclooxygenase (COX) pathway is important in modulating immune responses and is also a major target of nonsteroidal anti-inflammatory drugs (NSAIDs) and the newer COX-2 inhibitors. |
| 74 | 16272346 | The purpose of the present study was to examine the effect of deficiency of COX-1 or COX-2 on the host response to influenza. |
| 75 | 16272346 | We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice. |
| 76 | 16272346 | Infection induced less severe illness in COX-2-/- mice in comparison to WT and COX-1-/- mice as evidenced by body weight and body temperature changes. |
| 77 | 16272346 | COX-1-/- mice had enhanced inflammation and earlier appearance of proinflammatory cytokines in the BAL fluid, whereas the inflammatory and cytokine responses were blunted in COX-2-/- mice. |
| 78 | 16272346 | However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection. |
| 79 | 16272346 | Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection. |
| 80 | 16272346 | Thus, deficiency of COX-1 and COX-2 leads to contrasting effects in the host response to influenza infection, and these differences are associated with altered production of prostaglandins and leukotrienes following infection. |
| 81 | 16272346 | COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection. |
| 82 | 16272346 | Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection. |
| 83 | 16272346 | The cyclooxygenase (COX) pathway is important in modulating immune responses and is also a major target of nonsteroidal anti-inflammatory drugs (NSAIDs) and the newer COX-2 inhibitors. |
| 84 | 16272346 | The purpose of the present study was to examine the effect of deficiency of COX-1 or COX-2 on the host response to influenza. |
| 85 | 16272346 | We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice. |
| 86 | 16272346 | Infection induced less severe illness in COX-2-/- mice in comparison to WT and COX-1-/- mice as evidenced by body weight and body temperature changes. |
| 87 | 16272346 | COX-1-/- mice had enhanced inflammation and earlier appearance of proinflammatory cytokines in the BAL fluid, whereas the inflammatory and cytokine responses were blunted in COX-2-/- mice. |
| 88 | 16272346 | However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection. |
| 89 | 16272346 | Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection. |
| 90 | 16272346 | Thus, deficiency of COX-1 and COX-2 leads to contrasting effects in the host response to influenza infection, and these differences are associated with altered production of prostaglandins and leukotrienes following infection. |
| 91 | 16272346 | COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection. |
| 92 | 16272346 | Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection. |
| 93 | 16272346 | The cyclooxygenase (COX) pathway is important in modulating immune responses and is also a major target of nonsteroidal anti-inflammatory drugs (NSAIDs) and the newer COX-2 inhibitors. |
| 94 | 16272346 | The purpose of the present study was to examine the effect of deficiency of COX-1 or COX-2 on the host response to influenza. |
| 95 | 16272346 | We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice. |
| 96 | 16272346 | Infection induced less severe illness in COX-2-/- mice in comparison to WT and COX-1-/- mice as evidenced by body weight and body temperature changes. |
| 97 | 16272346 | COX-1-/- mice had enhanced inflammation and earlier appearance of proinflammatory cytokines in the BAL fluid, whereas the inflammatory and cytokine responses were blunted in COX-2-/- mice. |
| 98 | 16272346 | However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection. |
| 99 | 16272346 | Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection. |
| 100 | 16272346 | Thus, deficiency of COX-1 and COX-2 leads to contrasting effects in the host response to influenza infection, and these differences are associated with altered production of prostaglandins and leukotrienes following infection. |
| 101 | 16272346 | COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection. |
| 102 | 16272346 | Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection. |
| 103 | 16272346 | The cyclooxygenase (COX) pathway is important in modulating immune responses and is also a major target of nonsteroidal anti-inflammatory drugs (NSAIDs) and the newer COX-2 inhibitors. |
| 104 | 16272346 | The purpose of the present study was to examine the effect of deficiency of COX-1 or COX-2 on the host response to influenza. |
| 105 | 16272346 | We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice. |
| 106 | 16272346 | Infection induced less severe illness in COX-2-/- mice in comparison to WT and COX-1-/- mice as evidenced by body weight and body temperature changes. |
| 107 | 16272346 | COX-1-/- mice had enhanced inflammation and earlier appearance of proinflammatory cytokines in the BAL fluid, whereas the inflammatory and cytokine responses were blunted in COX-2-/- mice. |
| 108 | 16272346 | However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection. |
| 109 | 16272346 | Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection. |
| 110 | 16272346 | Thus, deficiency of COX-1 and COX-2 leads to contrasting effects in the host response to influenza infection, and these differences are associated with altered production of prostaglandins and leukotrienes following infection. |
| 111 | 16272346 | COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection. |
| 112 | 16272346 | Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection. |
| 113 | 16272346 | The cyclooxygenase (COX) pathway is important in modulating immune responses and is also a major target of nonsteroidal anti-inflammatory drugs (NSAIDs) and the newer COX-2 inhibitors. |
| 114 | 16272346 | The purpose of the present study was to examine the effect of deficiency of COX-1 or COX-2 on the host response to influenza. |
| 115 | 16272346 | We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice. |
| 116 | 16272346 | Infection induced less severe illness in COX-2-/- mice in comparison to WT and COX-1-/- mice as evidenced by body weight and body temperature changes. |
| 117 | 16272346 | COX-1-/- mice had enhanced inflammation and earlier appearance of proinflammatory cytokines in the BAL fluid, whereas the inflammatory and cytokine responses were blunted in COX-2-/- mice. |
| 118 | 16272346 | However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection. |
| 119 | 16272346 | Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection. |
| 120 | 16272346 | Thus, deficiency of COX-1 and COX-2 leads to contrasting effects in the host response to influenza infection, and these differences are associated with altered production of prostaglandins and leukotrienes following infection. |
| 121 | 16272346 | COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection. |
| 122 | 16272346 | Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection. |
| 123 | 16272346 | The cyclooxygenase (COX) pathway is important in modulating immune responses and is also a major target of nonsteroidal anti-inflammatory drugs (NSAIDs) and the newer COX-2 inhibitors. |
| 124 | 16272346 | The purpose of the present study was to examine the effect of deficiency of COX-1 or COX-2 on the host response to influenza. |
| 125 | 16272346 | We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice. |
| 126 | 16272346 | Infection induced less severe illness in COX-2-/- mice in comparison to WT and COX-1-/- mice as evidenced by body weight and body temperature changes. |
| 127 | 16272346 | COX-1-/- mice had enhanced inflammation and earlier appearance of proinflammatory cytokines in the BAL fluid, whereas the inflammatory and cytokine responses were blunted in COX-2-/- mice. |
| 128 | 16272346 | However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection. |
| 129 | 16272346 | Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection. |
| 130 | 16272346 | Thus, deficiency of COX-1 and COX-2 leads to contrasting effects in the host response to influenza infection, and these differences are associated with altered production of prostaglandins and leukotrienes following infection. |
| 131 | 16272346 | COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection. |
| 132 | 16272346 | Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection. |
| 133 | 16272346 | The cyclooxygenase (COX) pathway is important in modulating immune responses and is also a major target of nonsteroidal anti-inflammatory drugs (NSAIDs) and the newer COX-2 inhibitors. |
| 134 | 16272346 | The purpose of the present study was to examine the effect of deficiency of COX-1 or COX-2 on the host response to influenza. |
| 135 | 16272346 | We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice. |
| 136 | 16272346 | Infection induced less severe illness in COX-2-/- mice in comparison to WT and COX-1-/- mice as evidenced by body weight and body temperature changes. |
| 137 | 16272346 | COX-1-/- mice had enhanced inflammation and earlier appearance of proinflammatory cytokines in the BAL fluid, whereas the inflammatory and cytokine responses were blunted in COX-2-/- mice. |
| 138 | 16272346 | However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection. |
| 139 | 16272346 | Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection. |
| 140 | 16272346 | Thus, deficiency of COX-1 and COX-2 leads to contrasting effects in the host response to influenza infection, and these differences are associated with altered production of prostaglandins and leukotrienes following infection. |
| 141 | 16272346 | COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection. |
| 142 | 16272346 | Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection. |
| 143 | 16272346 | The cyclooxygenase (COX) pathway is important in modulating immune responses and is also a major target of nonsteroidal anti-inflammatory drugs (NSAIDs) and the newer COX-2 inhibitors. |
| 144 | 16272346 | The purpose of the present study was to examine the effect of deficiency of COX-1 or COX-2 on the host response to influenza. |
| 145 | 16272346 | We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice. |
| 146 | 16272346 | Infection induced less severe illness in COX-2-/- mice in comparison to WT and COX-1-/- mice as evidenced by body weight and body temperature changes. |
| 147 | 16272346 | COX-1-/- mice had enhanced inflammation and earlier appearance of proinflammatory cytokines in the BAL fluid, whereas the inflammatory and cytokine responses were blunted in COX-2-/- mice. |
| 148 | 16272346 | However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection. |
| 149 | 16272346 | Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection. |
| 150 | 16272346 | Thus, deficiency of COX-1 and COX-2 leads to contrasting effects in the host response to influenza infection, and these differences are associated with altered production of prostaglandins and leukotrienes following infection. |
| 151 | 16272346 | COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection. |
| 152 | 16397045 | Tumor-derived cyclooxygenase-2 (COX-2) and its product, prostaglandin E2, exert strong immunoinhibitory effects that block dendritic cell function and CD4+ and CD8+ T-cell proliferation and function. |
| 153 | 16397045 | Increased immunocyte trafficking was likely mediated by the generation of a Th1-type tumor microenvironment because COX-2 inhibition increased expression levels of mRNA for IFN-gamma, interleukin-12, IP-10, and MIG while lowering the expression of vascular endothelial growth factor within tumors. |
| 154 | 16397045 | Tumor-derived cyclooxygenase-2 (COX-2) and its product, prostaglandin E2, exert strong immunoinhibitory effects that block dendritic cell function and CD4+ and CD8+ T-cell proliferation and function. |
| 155 | 16397045 | Increased immunocyte trafficking was likely mediated by the generation of a Th1-type tumor microenvironment because COX-2 inhibition increased expression levels of mRNA for IFN-gamma, interleukin-12, IP-10, and MIG while lowering the expression of vascular endothelial growth factor within tumors. |
| 156 | 16822852 | Previous studies have shown that prostaglandin E(2) (PGE(2)) release by splenic F4/80(+) cyclooxygenase (COX)-2(+) macrophages (MØ) isolated from mice, treated with mycobacterial components, plays a major role in the regulation of immune responses. |
| 157 | 16822852 | However, splenic MØ, isolated from untreated mice and treated in vitro with lipopolysaccharide and interferon-gamma, express COX-1 and COX-2 within 1 day but release only minimal amounts of PGE(2) following elicitation with calcium ionophore A23187. |
| 158 | 16822852 | In sharp contrast, 14 days after HK-BCG treatment, PGE(2) release by COX-2(+) splenic MØ increased as much as sevenfold, and a greater increase was seen in IL-10(-/-) cells than in WT cells. |
| 159 | 16822852 | Previous studies have shown that prostaglandin E(2) (PGE(2)) release by splenic F4/80(+) cyclooxygenase (COX)-2(+) macrophages (MØ) isolated from mice, treated with mycobacterial components, plays a major role in the regulation of immune responses. |
| 160 | 16822852 | However, splenic MØ, isolated from untreated mice and treated in vitro with lipopolysaccharide and interferon-gamma, express COX-1 and COX-2 within 1 day but release only minimal amounts of PGE(2) following elicitation with calcium ionophore A23187. |
| 161 | 16822852 | In sharp contrast, 14 days after HK-BCG treatment, PGE(2) release by COX-2(+) splenic MØ increased as much as sevenfold, and a greater increase was seen in IL-10(-/-) cells than in WT cells. |
| 162 | 16822852 | Previous studies have shown that prostaglandin E(2) (PGE(2)) release by splenic F4/80(+) cyclooxygenase (COX)-2(+) macrophages (MØ) isolated from mice, treated with mycobacterial components, plays a major role in the regulation of immune responses. |
| 163 | 16822852 | However, splenic MØ, isolated from untreated mice and treated in vitro with lipopolysaccharide and interferon-gamma, express COX-1 and COX-2 within 1 day but release only minimal amounts of PGE(2) following elicitation with calcium ionophore A23187. |
| 164 | 16822852 | In sharp contrast, 14 days after HK-BCG treatment, PGE(2) release by COX-2(+) splenic MØ increased as much as sevenfold, and a greater increase was seen in IL-10(-/-) cells than in WT cells. |
| 165 | 17159912 | CpG-ODN induces the expression of cyclooxygenase (COX)-2, and its product prostaglandin (PG) E2 underlies an immunosuppressive network, therefore it is a simple strategy to use a COX-2 inhibitor for tumor vaccination with CpG-ODN. |
| 166 | 17464165 | Cyclo-oxygenase (COX)-2 inhibitors are also alleged to have a function in interrupting the development of HCC. |
| 167 | 17473370 | Vaccination efficacy can be amplified by depleting CD4;+CD25;+Foxp3;+ regulatory T cells (Treg), but the risk of inducing autoimmunity warrants new strategies to selectively amplify anti-tumor immunity when modulating Treg. |
| 168 | 17473370 | In the tumors, the major cyclooxygenase (COX)-2 product is prostaglandin E2(PGE2) which suppresses T and NK cells while amplifying Treg. |
| 169 | 17538120 | Upregulated genes included the immune regulatory molecules interleukin 1beta (IL-1beta), CIAS-1, tumor necrosis factor alpha, PDE4B, PTGS2, IL-8, CXCL2, CCL4, ICAM-1, CD83, GOS-2, IER3 (IEX-1), and TNFAIP3 (A20). |
| 170 | 17538120 | Plasma levels of IL-1beta and IL-8 were elevated during measles virus infection. |
| 171 | 17538120 | Downregulated genes mainly involved three gene ontology biological processes, transcription, signal transduction, and the immune response, and included IL-16 and cell surface receptors IL-4R, IL-6R, IL-7R, IL-27RA, CCR2, and CCR7. |
| 172 | 18479787 | Therapeutic vaccination with dendritic cells pulsed with tumor-derived Hsp70 and a COX-2 inhibitor induces protective immunity against B16 melanoma. |
| 173 | 18479787 | Here we sought to overcome this problem by therapeutic vaccination with dendritic cells (DC) pulsed with Hsp70 and a COX-2 inhibitor. |
| 174 | 18479787 | We found that Hsp70 induces IL-6 and IL-10 production and suppressed expression of CD40 on DC. |
| 175 | 18479787 | Incubation of DC with tumor-conditioned medium attenuated Hsp70-induced expression of CD80 and induced expression of COX-2. |
| 176 | 18479787 | Inhibition of COX-2 partially reversed the stimulatory effect of Hsp70 on DC IL-6 and IL-10 production and enhanced expression of CD80 and MHC classes I and II. |
| 177 | 18479787 | Therapeutic administration of DC pulsed in vitro with Hsp70 in the presence of a COX-2 inhibitor significantly reduced progression of B16 tumors in mice and significantly enhanced survival. |
| 178 | 18479787 | This was associated with a reduction in the frequency of IL-10-producing CD4(+) T cells and enhancement of IFN-gamma-producing CD8(+) T cells. |
| 179 | 18479787 | Therapeutic vaccination with dendritic cells pulsed with tumor-derived Hsp70 and a COX-2 inhibitor induces protective immunity against B16 melanoma. |
| 180 | 18479787 | Here we sought to overcome this problem by therapeutic vaccination with dendritic cells (DC) pulsed with Hsp70 and a COX-2 inhibitor. |
| 181 | 18479787 | We found that Hsp70 induces IL-6 and IL-10 production and suppressed expression of CD40 on DC. |
| 182 | 18479787 | Incubation of DC with tumor-conditioned medium attenuated Hsp70-induced expression of CD80 and induced expression of COX-2. |
| 183 | 18479787 | Inhibition of COX-2 partially reversed the stimulatory effect of Hsp70 on DC IL-6 and IL-10 production and enhanced expression of CD80 and MHC classes I and II. |
| 184 | 18479787 | Therapeutic administration of DC pulsed in vitro with Hsp70 in the presence of a COX-2 inhibitor significantly reduced progression of B16 tumors in mice and significantly enhanced survival. |
| 185 | 18479787 | This was associated with a reduction in the frequency of IL-10-producing CD4(+) T cells and enhancement of IFN-gamma-producing CD8(+) T cells. |
| 186 | 18479787 | Therapeutic vaccination with dendritic cells pulsed with tumor-derived Hsp70 and a COX-2 inhibitor induces protective immunity against B16 melanoma. |
| 187 | 18479787 | Here we sought to overcome this problem by therapeutic vaccination with dendritic cells (DC) pulsed with Hsp70 and a COX-2 inhibitor. |
| 188 | 18479787 | We found that Hsp70 induces IL-6 and IL-10 production and suppressed expression of CD40 on DC. |
| 189 | 18479787 | Incubation of DC with tumor-conditioned medium attenuated Hsp70-induced expression of CD80 and induced expression of COX-2. |
| 190 | 18479787 | Inhibition of COX-2 partially reversed the stimulatory effect of Hsp70 on DC IL-6 and IL-10 production and enhanced expression of CD80 and MHC classes I and II. |
| 191 | 18479787 | Therapeutic administration of DC pulsed in vitro with Hsp70 in the presence of a COX-2 inhibitor significantly reduced progression of B16 tumors in mice and significantly enhanced survival. |
| 192 | 18479787 | This was associated with a reduction in the frequency of IL-10-producing CD4(+) T cells and enhancement of IFN-gamma-producing CD8(+) T cells. |
| 193 | 18479787 | Therapeutic vaccination with dendritic cells pulsed with tumor-derived Hsp70 and a COX-2 inhibitor induces protective immunity against B16 melanoma. |
| 194 | 18479787 | Here we sought to overcome this problem by therapeutic vaccination with dendritic cells (DC) pulsed with Hsp70 and a COX-2 inhibitor. |
| 195 | 18479787 | We found that Hsp70 induces IL-6 and IL-10 production and suppressed expression of CD40 on DC. |
| 196 | 18479787 | Incubation of DC with tumor-conditioned medium attenuated Hsp70-induced expression of CD80 and induced expression of COX-2. |
| 197 | 18479787 | Inhibition of COX-2 partially reversed the stimulatory effect of Hsp70 on DC IL-6 and IL-10 production and enhanced expression of CD80 and MHC classes I and II. |
| 198 | 18479787 | Therapeutic administration of DC pulsed in vitro with Hsp70 in the presence of a COX-2 inhibitor significantly reduced progression of B16 tumors in mice and significantly enhanced survival. |
| 199 | 18479787 | This was associated with a reduction in the frequency of IL-10-producing CD4(+) T cells and enhancement of IFN-gamma-producing CD8(+) T cells. |
| 200 | 18479787 | Therapeutic vaccination with dendritic cells pulsed with tumor-derived Hsp70 and a COX-2 inhibitor induces protective immunity against B16 melanoma. |
| 201 | 18479787 | Here we sought to overcome this problem by therapeutic vaccination with dendritic cells (DC) pulsed with Hsp70 and a COX-2 inhibitor. |
| 202 | 18479787 | We found that Hsp70 induces IL-6 and IL-10 production and suppressed expression of CD40 on DC. |
| 203 | 18479787 | Incubation of DC with tumor-conditioned medium attenuated Hsp70-induced expression of CD80 and induced expression of COX-2. |
| 204 | 18479787 | Inhibition of COX-2 partially reversed the stimulatory effect of Hsp70 on DC IL-6 and IL-10 production and enhanced expression of CD80 and MHC classes I and II. |
| 205 | 18479787 | Therapeutic administration of DC pulsed in vitro with Hsp70 in the presence of a COX-2 inhibitor significantly reduced progression of B16 tumors in mice and significantly enhanced survival. |
| 206 | 18479787 | This was associated with a reduction in the frequency of IL-10-producing CD4(+) T cells and enhancement of IFN-gamma-producing CD8(+) T cells. |
| 207 | 18572242 | Nine cytokine genes (IL-2, -4, -10, -12, -13, -18, TNFalpha, TGFbeta and IFNgamma) and Cox-2 were selected for analysis. |
| 208 | 19097981 | After administration, whole lungs of C57Bl/6 mice were lavaged with saline; COX-2 expression and PGE(2) release by alveolar MØ and tumor necrosis factor (TNF)-alpha and nitric oxide levels in the lung lavage were monitored. |
| 209 | 19140872 | Our results demonstrates that Mycobacterium bovis BCG (M. bovis BCG) downregulates tumour necrosis factor-alpha (TNF-alpha)-induced COX-2 gene expression in alveolar epithelial cells by inhibiting the phosphorylations of Raf-1 and p38 kinases. |
| 210 | 19140872 | Further, M. bovis BCG-mediated inhibition of COX-2 or p38 mitogen-activated protein kinase could be reversed by Calyculin A, a selective inhibitor of Ser/Thr phosphatases. |
| 211 | 19140872 | Moreover, M. bovis BCG inhibited the TNF-alpha-triggered NF-kappaB activation following IkappaB degradation. |
| 212 | 19140872 | Our results demonstrates that Mycobacterium bovis BCG (M. bovis BCG) downregulates tumour necrosis factor-alpha (TNF-alpha)-induced COX-2 gene expression in alveolar epithelial cells by inhibiting the phosphorylations of Raf-1 and p38 kinases. |
| 213 | 19140872 | Further, M. bovis BCG-mediated inhibition of COX-2 or p38 mitogen-activated protein kinase could be reversed by Calyculin A, a selective inhibitor of Ser/Thr phosphatases. |
| 214 | 19140872 | Moreover, M. bovis BCG inhibited the TNF-alpha-triggered NF-kappaB activation following IkappaB degradation. |
| 215 | 19345936 | The widely used non-steroidal anti-inflammatory drugs (NSAIDs) function mainly through inhibition of cyclooxygenases 1 and 2 (Cox-1 and Cox-2). |
| 216 | 19345936 | Unlike Cox-1, Cox-2 is considered an inducible and pro-inflammatory enzyme. |
| 217 | 19345936 | Herein, we tested a variety of Cox-1/Cox-2 non-selective NSAIDs, namely ibuprofen, tylenol, aspirin and naproxen and report that they blunt IgM and IgG synthesis in stimulated human peripheral blood mononuclear cells (PBMC). |
| 218 | 19345936 | The widely used non-steroidal anti-inflammatory drugs (NSAIDs) function mainly through inhibition of cyclooxygenases 1 and 2 (Cox-1 and Cox-2). |
| 219 | 19345936 | Unlike Cox-1, Cox-2 is considered an inducible and pro-inflammatory enzyme. |
| 220 | 19345936 | Herein, we tested a variety of Cox-1/Cox-2 non-selective NSAIDs, namely ibuprofen, tylenol, aspirin and naproxen and report that they blunt IgM and IgG synthesis in stimulated human peripheral blood mononuclear cells (PBMC). |
| 221 | 19345936 | The widely used non-steroidal anti-inflammatory drugs (NSAIDs) function mainly through inhibition of cyclooxygenases 1 and 2 (Cox-1 and Cox-2). |
| 222 | 19345936 | Unlike Cox-1, Cox-2 is considered an inducible and pro-inflammatory enzyme. |
| 223 | 19345936 | Herein, we tested a variety of Cox-1/Cox-2 non-selective NSAIDs, namely ibuprofen, tylenol, aspirin and naproxen and report that they blunt IgM and IgG synthesis in stimulated human peripheral blood mononuclear cells (PBMC). |
| 224 | 19414123 | There is potential utility for antifibrinolytic drugs, cytokine supplementation (IL2/IFN), and Cox-2 inhibitors. |
| 225 | 20050331 | We demonstrate that the Cox-2 selective small molecule inhibitors SC-58125 and NS-398 attenuate the production of human antibody isotypes including immunoglobulin M (IgM), IgG1, IgG2, IgG3 and IgG4. |
| 226 | 20050331 | In addition, inhibition of Cox-2 significantly reduced the generation of CD38+ IgM+ and CD38+ IgG+ antibody-secreting cells. |
| 227 | 20050331 | Interestingly, we discovered that inhibition of Cox-2 activity in normal human B cells severely reduced the messenger RNA and protein levels of the essential plasma cell transcription factor, Blimp-1. |
| 228 | 20050331 | These observations were mirrored in Cox-2-deficient mice, which had reduced CD138+ plasma cells and a near loss of Blimp-1 expression. |
| 229 | 20050331 | We demonstrate that the Cox-2 selective small molecule inhibitors SC-58125 and NS-398 attenuate the production of human antibody isotypes including immunoglobulin M (IgM), IgG1, IgG2, IgG3 and IgG4. |
| 230 | 20050331 | In addition, inhibition of Cox-2 significantly reduced the generation of CD38+ IgM+ and CD38+ IgG+ antibody-secreting cells. |
| 231 | 20050331 | Interestingly, we discovered that inhibition of Cox-2 activity in normal human B cells severely reduced the messenger RNA and protein levels of the essential plasma cell transcription factor, Blimp-1. |
| 232 | 20050331 | These observations were mirrored in Cox-2-deficient mice, which had reduced CD138+ plasma cells and a near loss of Blimp-1 expression. |
| 233 | 20050331 | We demonstrate that the Cox-2 selective small molecule inhibitors SC-58125 and NS-398 attenuate the production of human antibody isotypes including immunoglobulin M (IgM), IgG1, IgG2, IgG3 and IgG4. |
| 234 | 20050331 | In addition, inhibition of Cox-2 significantly reduced the generation of CD38+ IgM+ and CD38+ IgG+ antibody-secreting cells. |
| 235 | 20050331 | Interestingly, we discovered that inhibition of Cox-2 activity in normal human B cells severely reduced the messenger RNA and protein levels of the essential plasma cell transcription factor, Blimp-1. |
| 236 | 20050331 | These observations were mirrored in Cox-2-deficient mice, which had reduced CD138+ plasma cells and a near loss of Blimp-1 expression. |
| 237 | 20050331 | We demonstrate that the Cox-2 selective small molecule inhibitors SC-58125 and NS-398 attenuate the production of human antibody isotypes including immunoglobulin M (IgM), IgG1, IgG2, IgG3 and IgG4. |
| 238 | 20050331 | In addition, inhibition of Cox-2 significantly reduced the generation of CD38+ IgM+ and CD38+ IgG+ antibody-secreting cells. |
| 239 | 20050331 | Interestingly, we discovered that inhibition of Cox-2 activity in normal human B cells severely reduced the messenger RNA and protein levels of the essential plasma cell transcription factor, Blimp-1. |
| 240 | 20050331 | These observations were mirrored in Cox-2-deficient mice, which had reduced CD138+ plasma cells and a near loss of Blimp-1 expression. |
| 241 | 22679002 | MyD88(-/-) mouse tissues also had fewer submucosal fibroblasts and 60% less collagen. |
| 242 | 22679002 | We noted that cyclooxygenase (Cox)-2 expression was MyD88-dependent, with numerous Cox-2-positive cells identified in fibrotic regions of WT mice at postinfection day 7, but not in MyD88(-/-) mice. |
| 243 | 22679002 | Treatment of WT mice with the Cox-2 inhibitor rofecoxib (20 mg/kg) significantly reduced fibroblast numbers and collagen levels without altering colitis severity. |
| 244 | 22679002 | In conclusion, MyD88 and Cox-2 signaling play roles in intestinal fibrosis during Salmonella-induced enterocolitis. |
| 245 | 22679002 | MyD88(-/-) mouse tissues also had fewer submucosal fibroblasts and 60% less collagen. |
| 246 | 22679002 | We noted that cyclooxygenase (Cox)-2 expression was MyD88-dependent, with numerous Cox-2-positive cells identified in fibrotic regions of WT mice at postinfection day 7, but not in MyD88(-/-) mice. |
| 247 | 22679002 | Treatment of WT mice with the Cox-2 inhibitor rofecoxib (20 mg/kg) significantly reduced fibroblast numbers and collagen levels without altering colitis severity. |
| 248 | 22679002 | In conclusion, MyD88 and Cox-2 signaling play roles in intestinal fibrosis during Salmonella-induced enterocolitis. |
| 249 | 22679002 | MyD88(-/-) mouse tissues also had fewer submucosal fibroblasts and 60% less collagen. |
| 250 | 22679002 | We noted that cyclooxygenase (Cox)-2 expression was MyD88-dependent, with numerous Cox-2-positive cells identified in fibrotic regions of WT mice at postinfection day 7, but not in MyD88(-/-) mice. |
| 251 | 22679002 | Treatment of WT mice with the Cox-2 inhibitor rofecoxib (20 mg/kg) significantly reduced fibroblast numbers and collagen levels without altering colitis severity. |
| 252 | 22679002 | In conclusion, MyD88 and Cox-2 signaling play roles in intestinal fibrosis during Salmonella-induced enterocolitis. |
| 253 | 23271799 | This review will examine mechanisms in which TLR activation upregulates protumorigenic pathways, including the induction of inducible nitric oxide synthase (iNOS2) and COX2, which in turn increase TLR expression and promote a feed-forward loop leading to tumor progression and the development of more aggressive tumor phenotypes. |
| 254 | 23354599 | We found that alphα-synuclein (α-syn) antibody significantly increased, IL-4 increased and IFN-r reduced in the serum of immunized C57BL/6 mice in optimized DNA vaccine group. |
| 255 | 23354599 | The preventive immunization with optimized DNA vaccine made the motor symptoms improved significantly, the apoptosis of tyrosine hydroxylase (TH) neuron and cyclooxygenase-2 (COX-2) expression significantly decreased in MPTP model mice. |
| 256 | 23536693 | Mycoplasma fermentans MALP-2 induces heme oxygenase-1 expression via mitogen-activated protein kinases and Nrf2 pathways to modulate cyclooxygenase 2 expression in human monocytes. |
| 257 | 23536693 | Specific inhibitors of mitogen-activated protein kinases (MAPKs), SB203580, PD98059, and SP600125, significantly abolished HO-1 expression. |
| 258 | 23536693 | In addition, MALP-2 also induced NF-E2-related factor 2 (Nrf2) translocation, and the silencing of Nrf2 expression in THP-1 cells decreased the levels of MALP-2-mediated HO-1 expression. |
| 259 | 23536693 | Furthermore, COX-2 protein expression levels were upregulated in THP-1 cells in response to MALP-2, and transfection with small interfering RNAs of HO-1 significantly increased COX-2 accumulation. |
| 260 | 23536693 | These results demonstrate that MALP-2 induces HO-1 expression via MAPKs and Nrf2 pathways and, furthermore, that MALP-2-induced COX-2 expression was modulated by HO-1 in THP-1 cells. |
| 261 | 23536693 | Mycoplasma fermentans MALP-2 induces heme oxygenase-1 expression via mitogen-activated protein kinases and Nrf2 pathways to modulate cyclooxygenase 2 expression in human monocytes. |
| 262 | 23536693 | Specific inhibitors of mitogen-activated protein kinases (MAPKs), SB203580, PD98059, and SP600125, significantly abolished HO-1 expression. |
| 263 | 23536693 | In addition, MALP-2 also induced NF-E2-related factor 2 (Nrf2) translocation, and the silencing of Nrf2 expression in THP-1 cells decreased the levels of MALP-2-mediated HO-1 expression. |
| 264 | 23536693 | Furthermore, COX-2 protein expression levels were upregulated in THP-1 cells in response to MALP-2, and transfection with small interfering RNAs of HO-1 significantly increased COX-2 accumulation. |
| 265 | 23536693 | These results demonstrate that MALP-2 induces HO-1 expression via MAPKs and Nrf2 pathways and, furthermore, that MALP-2-induced COX-2 expression was modulated by HO-1 in THP-1 cells. |
| 266 | 23600134 | TPs inhibit growth factor receptor-mediated signal transduction pathway, decrease the activities of mitogen activated protein kinases and activator protein transcription factor-1, block nuclear factor-kappaB signaling pathway, reduce proteasome activity, lower overexpression of COX-2, subside dihydrofolate reductase and telomerase, and inhibit DNA methylation and matrix metalloproteinases. |
| 267 | 23918793 | There is growing evidence that many of the most promising cancer chemoprevention agents including aspirin, COX-2 inhibitors, aromatase inhibitors, and bisphosphonates mediate their effects, in part, by enhancing immunosurveillance and reversing the immune evasive mechanisms that premalignant lesions use. |
| 268 | 24343645 | Janus kinase 3 activity is necessary for phosphorylation of cytosolic phospholipase A2 and prostaglandin E2 synthesis by macrophages infected with Francisella tularensis live vaccine strain. |
| 269 | 24343645 | The synthesis of PGE2 begins with the liberation of arachidonic acid (AA) from membrane phospholipids by cytosolic phospholipase A2 (cPLA2). |
| 270 | 24343645 | In this study, we show that cPLA2, p38 mitogen-activated protein kinase (MAPK), and Janus kinase 3 (JAK3) signaling are necessary for F. tularensis-induced PGE2 production. |
| 271 | 24343645 | Inhibition of JAK3 activity reduced the phosphorylation of cPLA2 and COX-2 protein levels. |
| 272 | 24343645 | In addition, JAK3 regulates cPLA2 phosphorylation independent of transcription. |
| 273 | 24343645 | Moreover, p38 MAPK activity is required for F. tularensis-induced COX-2 protein synthesis, but not for the phosphorylation of cPLA2. |
| 274 | 24343645 | This research highlights a unique signaling axis in which JAK3 and p38 MAPK regulate the activity of multiple enzymes of the PGE2-biosynthetic pathway in macrophages infected with F. tularensis. |
| 275 | 24343645 | Janus kinase 3 activity is necessary for phosphorylation of cytosolic phospholipase A2 and prostaglandin E2 synthesis by macrophages infected with Francisella tularensis live vaccine strain. |
| 276 | 24343645 | The synthesis of PGE2 begins with the liberation of arachidonic acid (AA) from membrane phospholipids by cytosolic phospholipase A2 (cPLA2). |
| 277 | 24343645 | In this study, we show that cPLA2, p38 mitogen-activated protein kinase (MAPK), and Janus kinase 3 (JAK3) signaling are necessary for F. tularensis-induced PGE2 production. |
| 278 | 24343645 | Inhibition of JAK3 activity reduced the phosphorylation of cPLA2 and COX-2 protein levels. |
| 279 | 24343645 | In addition, JAK3 regulates cPLA2 phosphorylation independent of transcription. |
| 280 | 24343645 | Moreover, p38 MAPK activity is required for F. tularensis-induced COX-2 protein synthesis, but not for the phosphorylation of cPLA2. |
| 281 | 24343645 | This research highlights a unique signaling axis in which JAK3 and p38 MAPK regulate the activity of multiple enzymes of the PGE2-biosynthetic pathway in macrophages infected with F. tularensis. |
| 282 | 24831259 | Expression of human papillomavirus is correlated with Ki-67 and COX-2 expressions in keratocystic odontogenic tumor. |
| 283 | 24831259 | The aim of the current study was to investigate the presence of human papillomavirus (HPV) and evaluate its association with Ki-67 and cyclooxygenase-2 (COX-2) expressions in keratocystic odontogenic tumor (KCOT). |
| 284 | 24831259 | Moreover, the expressions of Ki-67 and COX-2 proteins were analyzed immunohistochemically. |
| 285 | 24831259 | Expression of HPV-DNA was positively correlated with Ki-67 and COX-2 expressions (p < 0.05), whereas HPV-L1 positive staining was positively correlated with COX-2 (p < 0.05) and highly associated with those of Ki-67 (p < 0.01). |
| 286 | 24831259 | Expression of human papillomavirus is correlated with Ki-67 and COX-2 expressions in keratocystic odontogenic tumor. |
| 287 | 24831259 | The aim of the current study was to investigate the presence of human papillomavirus (HPV) and evaluate its association with Ki-67 and cyclooxygenase-2 (COX-2) expressions in keratocystic odontogenic tumor (KCOT). |
| 288 | 24831259 | Moreover, the expressions of Ki-67 and COX-2 proteins were analyzed immunohistochemically. |
| 289 | 24831259 | Expression of HPV-DNA was positively correlated with Ki-67 and COX-2 expressions (p < 0.05), whereas HPV-L1 positive staining was positively correlated with COX-2 (p < 0.05) and highly associated with those of Ki-67 (p < 0.01). |
| 290 | 24831259 | Expression of human papillomavirus is correlated with Ki-67 and COX-2 expressions in keratocystic odontogenic tumor. |
| 291 | 24831259 | The aim of the current study was to investigate the presence of human papillomavirus (HPV) and evaluate its association with Ki-67 and cyclooxygenase-2 (COX-2) expressions in keratocystic odontogenic tumor (KCOT). |
| 292 | 24831259 | Moreover, the expressions of Ki-67 and COX-2 proteins were analyzed immunohistochemically. |
| 293 | 24831259 | Expression of HPV-DNA was positively correlated with Ki-67 and COX-2 expressions (p < 0.05), whereas HPV-L1 positive staining was positively correlated with COX-2 (p < 0.05) and highly associated with those of Ki-67 (p < 0.01). |
| 294 | 24831259 | Expression of human papillomavirus is correlated with Ki-67 and COX-2 expressions in keratocystic odontogenic tumor. |
| 295 | 24831259 | The aim of the current study was to investigate the presence of human papillomavirus (HPV) and evaluate its association with Ki-67 and cyclooxygenase-2 (COX-2) expressions in keratocystic odontogenic tumor (KCOT). |
| 296 | 24831259 | Moreover, the expressions of Ki-67 and COX-2 proteins were analyzed immunohistochemically. |
| 297 | 24831259 | Expression of HPV-DNA was positively correlated with Ki-67 and COX-2 expressions (p < 0.05), whereas HPV-L1 positive staining was positively correlated with COX-2 (p < 0.05) and highly associated with those of Ki-67 (p < 0.01). |
| 298 | 25093281 | The experimental results indicated that urease activity, H. pylori colonisation density, the levels of IL-8 and TNF-α in the serum, and the levels of COX-2 and NAP in gastric tissue were significantly lower and the IgG level in the serum and the IFN-γ level in spleen lymphocytes were significantly higher in the vaccinated group compared with the model control group; additionally, gastric mucosal inflammation was notably alleviated following vaccination. |
| 299 | 25093281 | The expression levels of the microRNA-155 target proteins IFN-γRα, AID, and PU.1 were significantly down-regulated; these results indicated that CTB-UE induced an immune response biased towards Th1 cells by up-regulating microRNA-155 to inhibit IFN-γRα expression and induced a humoral immune response towards B cells by up-regulating microRNA-155 to inhibit PU.1 and AID expression. |
| 300 | 25118473 | Both calcitriol and the inhibition of COX-2 have shown antiproliferative and prodifferentiation, as well as pro-apoptotic effects in different malignancies in vitro and in vivo, and the key prostaglandin catabolic enzyme 15-hydroxyprostaglandin dehydrogenase (15-PGDH) is known to have tumor suppressor activity. |
| 301 | 25369453 | The production of eicosanoids from Arachidonic Acid (AA) can be hampered due to suppression of the enzyme phospholipase A2 by IL-4, an essential cytokine required for the differentiation of DCs. |
| 302 | 25369453 | Thus addition of AA to the culture media is skewing the DCs towards the secretion of more IL-12 and less of IL-10 along with the restoration of eicosanoids levels in a COX-2 mediated pathway thereby enhancing the functionality of these cells to be used as a potent cellular vaccine. |
| 303 | 25485483 | The immune associated genes, interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin 10 (IL-10), tumor necrosis factor-α (TNF-α), ciclo-oxigenase-2 (COX-2), and Mx gene were studied by real-time PCR in head-kidney leucocytes of sea bass after incubation with the extracellular products (ECPs) of the probiotic strain Vagococcus fluvialis L21 and polyinosinic:polycytidylic acid (POLY I:C), at different times (T1.5, T6, T12, T24, T48 and T72). |
| 304 | 25485483 | In general, we can observe how pro-inflammatory cytokines IL-1β, TNF-α, IL-6 and COX-2 studied displayed a strong peak after stimulation with 1.5 h of ECPs of V. fluvialis L21, significant differences (P < 0.05) exist with other periods and with the POLY I: C at the same time. |
| 305 | 25485483 | Similarly to the case of IL-10 also produced a statistically significant (P < 0.05) peak of expression on leukocytes that were stimulated with the ECPs of V. fluvialis L21. |
| 306 | 25485483 | The immune associated genes, interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin 10 (IL-10), tumor necrosis factor-α (TNF-α), ciclo-oxigenase-2 (COX-2), and Mx gene were studied by real-time PCR in head-kidney leucocytes of sea bass after incubation with the extracellular products (ECPs) of the probiotic strain Vagococcus fluvialis L21 and polyinosinic:polycytidylic acid (POLY I:C), at different times (T1.5, T6, T12, T24, T48 and T72). |
| 307 | 25485483 | In general, we can observe how pro-inflammatory cytokines IL-1β, TNF-α, IL-6 and COX-2 studied displayed a strong peak after stimulation with 1.5 h of ECPs of V. fluvialis L21, significant differences (P < 0.05) exist with other periods and with the POLY I: C at the same time. |
| 308 | 25485483 | Similarly to the case of IL-10 also produced a statistically significant (P < 0.05) peak of expression on leukocytes that were stimulated with the ECPs of V. fluvialis L21. |
| 309 | 26118933 | Five genes encoding for five different molecules were analyzed by real time PCR: IL-1β, IL Ir-2, Cox-2, Mx and TNFα. |
| 310 | 26118933 | Results show that the heat-inactivated vaccine stimulates the up-regulation of IL-1β, IL Ir-2, Cox-2 and TNFα genes whereas the UV-light inactivated vaccine was the unique vaccine which stimulates the expression of Mx gene. |
| 311 | 26118933 | Five genes encoding for five different molecules were analyzed by real time PCR: IL-1β, IL Ir-2, Cox-2, Mx and TNFα. |
| 312 | 26118933 | Results show that the heat-inactivated vaccine stimulates the up-regulation of IL-1β, IL Ir-2, Cox-2 and TNFα genes whereas the UV-light inactivated vaccine was the unique vaccine which stimulates the expression of Mx gene. |
| 313 | 26282681 | With respect to immune-related genes, IL-1β, COX-2, iNOS, and IL-10 were highly (P < 0.05) up-regulated in fish immunized with cellular components, compared to the control. |
| 314 | 26391398 | Ac2PIM-responsive miR-150 and miR-143 target receptor-interacting protein kinase 2 and transforming growth factor beta-activated kinase 1 to suppress NOD2-induced immunomodulators. |
| 315 | 26391398 | While Ac2PIM treatment of macrophages compromised their ability to induce NOD2-dependent immunomodulators like cyclooxygenase (COX)-2, suppressor of cytokine signaling (SOCS)-3, and matrix metalloproteinase (MMP)-9, no change in the NOD2-responsive NO, TNF-α, VEGF-A, and IL-12 levels was observed. |
| 316 | 26391398 | Further, genome-wide microRNA expression profiling identified Ac2PIM-responsive miR-150 and miR-143 to target NOD2 signaling adaptors, RIP2 and TAK1, respectively. |
| 317 | 26391398 | Interestingly, Ac2PIM was found to activate the SRC-FAK-PYK2-CREB cascade via TLR2 to recruit CBP/P300 at the promoters of miR-150 and miR-143 and epigenetically induce their expression. |
| 318 | 26391398 | Loss-of-function studies utilizing specific miRNA inhibitors establish that Ac2PIM, via the miRNAs, abrogate NOD2-induced PI3K-PKCδ-MAPK pathway to suppress β-catenin-mediated expression of COX-2, SOCS-3, and MMP-9. |
| 319 | 26391398 | Ac2PIM-responsive miR-150 and miR-143 target receptor-interacting protein kinase 2 and transforming growth factor beta-activated kinase 1 to suppress NOD2-induced immunomodulators. |
| 320 | 26391398 | While Ac2PIM treatment of macrophages compromised their ability to induce NOD2-dependent immunomodulators like cyclooxygenase (COX)-2, suppressor of cytokine signaling (SOCS)-3, and matrix metalloproteinase (MMP)-9, no change in the NOD2-responsive NO, TNF-α, VEGF-A, and IL-12 levels was observed. |
| 321 | 26391398 | Further, genome-wide microRNA expression profiling identified Ac2PIM-responsive miR-150 and miR-143 to target NOD2 signaling adaptors, RIP2 and TAK1, respectively. |
| 322 | 26391398 | Interestingly, Ac2PIM was found to activate the SRC-FAK-PYK2-CREB cascade via TLR2 to recruit CBP/P300 at the promoters of miR-150 and miR-143 and epigenetically induce their expression. |
| 323 | 26391398 | Loss-of-function studies utilizing specific miRNA inhibitors establish that Ac2PIM, via the miRNAs, abrogate NOD2-induced PI3K-PKCδ-MAPK pathway to suppress β-catenin-mediated expression of COX-2, SOCS-3, and MMP-9. |