Ignet

Gene Information

Gene symbol: PTGS1

Gene name: prostaglandin-endoperoxide synthase 1 (prostaglandin G/H synthase and cyclooxygenase)

HGNC ID: 9604

Synonyms: COX1, PGHS-1, PTGHS

Related Genes

#	Gene Symbol	Number of hits
1	CA1	1 hits
2	CA3	1 hits
3	COX8A	1 hits
4	IFNG	1 hits
5	PTGES	1 hits
6	PTGS2	1 hits
7	TNF	1 hits

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	12949405	Cyclooxygenase (COX) enzymes catalyze the synthesis of prostaglandins and exist as two isoforms, COX-1 and COX-2.
6	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.
7	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.
8	16204627	Cultures of spleen cells isolated from these mice expressed interleukin (IL)-4 and IL-10 in recall responses.
9	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.
10	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.
11	16272346	Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection.
12	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.
13	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.
14	16272346	We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice.
15	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.
16	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.
17	16272346	However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection.
18	16272346	Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection.
19	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.
20	16272346	COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection.
21	16272346	Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection.
22	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.
23	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.
24	16272346	We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice.
25	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.
26	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.
27	16272346	However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection.
28	16272346	Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection.
29	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.
30	16272346	COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection.
31	16272346	Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection.
32	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.
33	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.
34	16272346	We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice.
35	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.
36	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.
37	16272346	However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection.
38	16272346	Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection.
39	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.
40	16272346	COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection.
41	16272346	Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection.
42	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.
43	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.
44	16272346	We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice.
45	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.
46	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.
47	16272346	However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection.
48	16272346	Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection.
49	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.
50	16272346	COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection.
51	16272346	Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection.
52	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.
53	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.
54	16272346	We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice.
55	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.
56	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.
57	16272346	However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection.
58	16272346	Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection.
59	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.
60	16272346	COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection.
61	16272346	Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection.
62	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.
63	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.
64	16272346	We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice.
65	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.
66	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.
67	16272346	However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection.
68	16272346	Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection.
69	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.
70	16272346	COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection.
71	16272346	Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection.
72	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.
73	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.
74	16272346	We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice.
75	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.
76	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.
77	16272346	However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection.
78	16272346	Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection.
79	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.
80	16272346	COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection.
81	16272346	Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection.
82	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.
83	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.
84	16272346	We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice.
85	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.
86	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.
87	16272346	However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection.
88	16272346	Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection.
89	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.
90	16272346	COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection.
91	16272346	Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection.
92	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.
93	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.
94	16272346	We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice.
95	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.
96	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.
97	16272346	However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection.
98	16272346	Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection.
99	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.
100	16272346	COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection.
101	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.
102	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.
103	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.
104	19345936	The widely used non-steroidal anti-inflammatory drugs (NSAIDs) function mainly through inhibition of cyclooxygenases 1 and 2 (Cox-1 and Cox-2).
105	19345936	Unlike Cox-1, Cox-2 is considered an inducible and pro-inflammatory enzyme.
106	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).
107	19345936	The widely used non-steroidal anti-inflammatory drugs (NSAIDs) function mainly through inhibition of cyclooxygenases 1 and 2 (Cox-1 and Cox-2).
108	19345936	Unlike Cox-1, Cox-2 is considered an inducible and pro-inflammatory enzyme.
109	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).
110	19345936	The widely used non-steroidal anti-inflammatory drugs (NSAIDs) function mainly through inhibition of cyclooxygenases 1 and 2 (Cox-1 and Cox-2).
111	19345936	Unlike Cox-1, Cox-2 is considered an inducible and pro-inflammatory enzyme.
112	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).
113	25101545	Fluoxetine administered in drinking water at a dose of 80 mg/l, 5 days before BCG and for 2 more weeks resulted in significant decrease in total immobility time during FST and TST and in cerebral PGE2 and NO levels.
114	25101545	Both ibuprofen (200 mg/l) and L-NAME (1 g/l) administered in drinking water 24 h before BCG and for 2 more weeks resulted in decrease in the total immobility time during FST and TST and in cerebral PGE2 and NO levels, which was comparable to fluoxetine's effect.
115	25101545	On the other hand, l-arginine administered at a dose of 6 g/l in drinking water together with ibuprofen or fluoxetine reversed their effect on FST, TST and cerebral PGE2 and NO levels.
116	25101545	Immunohistochemistry showed a decrease in COX-1 and i-NOS immunoreactivity in the CA1 and CA3 areas of the hippocampus following ibuprofen treatment.