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PMID |
Sentence |
1 |
19404546
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Here, we present novel insights into the participation of DV in the downregulation of the thrombomodulin-thrombin-protein C complex formation at the endothelial surface, with a reduction in activated protein C (APC).
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2 |
19404546
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APC is the most important vasoprotective protein because it downregulates thrombin generation (by the inactivation of procoagulant factors Va and VIIIa) and has anti-inflammatory, antiapoptotic, and barrier protection properties.
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3 |
19404546
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These biological functions of APC are associated with the endothelial protein C receptor (EPCR) and protease-activated receptor 1 (PAR-1) signalling pathways, which link the coagulation-inflammation responses.
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4 |
24015257
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Herein, the effects of a PAR1 agonist and a PAR1 antagonist on hMPV infection were investigated in BALB/c mice.
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5 |
24015257
|
Intranasal administration of the PAR1 agonist resulted in increased weight loss and mortality of infected mice.
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6 |
24015257
|
Conversely, the PAR1 antagonist was beneficial to hMPV infection by decreasing weight loss and clinical signs and by significantly reducing pulmonary inflammation, pro-inflammatory cytokine levels (including IL-6, KC and MCP-1) and recruitment of immune cells to the lungs.
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7 |
24015257
|
In addition, a significant reduction in pulmonary viral titers was also observed in the lungs of PAR1 antagonist-treated mice.
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8 |
24015257
|
Despite no apparent direct effect on virus replication during in vitro experiments, an important role for PAR1 in the regulation of furin expression in the lungs was shown for the first time.
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9 |
24015257
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Further experiments indicated that the hMPV fusion protein can be cleaved by furin thus suggesting that PAR1 could have an effect on viral infectivity in addition to its immunomodulatory properties.
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10 |
24015257
|
Thus, inhibition of PAR1 by selected antagonists could represent an interesting strategy for decreasing the severity of paramyxovirus infections.
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11 |
24015257
|
Herein, the effects of a PAR1 agonist and a PAR1 antagonist on hMPV infection were investigated in BALB/c mice.
|
12 |
24015257
|
Intranasal administration of the PAR1 agonist resulted in increased weight loss and mortality of infected mice.
|
13 |
24015257
|
Conversely, the PAR1 antagonist was beneficial to hMPV infection by decreasing weight loss and clinical signs and by significantly reducing pulmonary inflammation, pro-inflammatory cytokine levels (including IL-6, KC and MCP-1) and recruitment of immune cells to the lungs.
|
14 |
24015257
|
In addition, a significant reduction in pulmonary viral titers was also observed in the lungs of PAR1 antagonist-treated mice.
|
15 |
24015257
|
Despite no apparent direct effect on virus replication during in vitro experiments, an important role for PAR1 in the regulation of furin expression in the lungs was shown for the first time.
|
16 |
24015257
|
Further experiments indicated that the hMPV fusion protein can be cleaved by furin thus suggesting that PAR1 could have an effect on viral infectivity in addition to its immunomodulatory properties.
|
17 |
24015257
|
Thus, inhibition of PAR1 by selected antagonists could represent an interesting strategy for decreasing the severity of paramyxovirus infections.
|
18 |
24015257
|
Herein, the effects of a PAR1 agonist and a PAR1 antagonist on hMPV infection were investigated in BALB/c mice.
|
19 |
24015257
|
Intranasal administration of the PAR1 agonist resulted in increased weight loss and mortality of infected mice.
|
20 |
24015257
|
Conversely, the PAR1 antagonist was beneficial to hMPV infection by decreasing weight loss and clinical signs and by significantly reducing pulmonary inflammation, pro-inflammatory cytokine levels (including IL-6, KC and MCP-1) and recruitment of immune cells to the lungs.
|
21 |
24015257
|
In addition, a significant reduction in pulmonary viral titers was also observed in the lungs of PAR1 antagonist-treated mice.
|
22 |
24015257
|
Despite no apparent direct effect on virus replication during in vitro experiments, an important role for PAR1 in the regulation of furin expression in the lungs was shown for the first time.
|
23 |
24015257
|
Further experiments indicated that the hMPV fusion protein can be cleaved by furin thus suggesting that PAR1 could have an effect on viral infectivity in addition to its immunomodulatory properties.
|
24 |
24015257
|
Thus, inhibition of PAR1 by selected antagonists could represent an interesting strategy for decreasing the severity of paramyxovirus infections.
|
25 |
24015257
|
Herein, the effects of a PAR1 agonist and a PAR1 antagonist on hMPV infection were investigated in BALB/c mice.
|
26 |
24015257
|
Intranasal administration of the PAR1 agonist resulted in increased weight loss and mortality of infected mice.
|
27 |
24015257
|
Conversely, the PAR1 antagonist was beneficial to hMPV infection by decreasing weight loss and clinical signs and by significantly reducing pulmonary inflammation, pro-inflammatory cytokine levels (including IL-6, KC and MCP-1) and recruitment of immune cells to the lungs.
|
28 |
24015257
|
In addition, a significant reduction in pulmonary viral titers was also observed in the lungs of PAR1 antagonist-treated mice.
|
29 |
24015257
|
Despite no apparent direct effect on virus replication during in vitro experiments, an important role for PAR1 in the regulation of furin expression in the lungs was shown for the first time.
|
30 |
24015257
|
Further experiments indicated that the hMPV fusion protein can be cleaved by furin thus suggesting that PAR1 could have an effect on viral infectivity in addition to its immunomodulatory properties.
|
31 |
24015257
|
Thus, inhibition of PAR1 by selected antagonists could represent an interesting strategy for decreasing the severity of paramyxovirus infections.
|
32 |
24015257
|
Herein, the effects of a PAR1 agonist and a PAR1 antagonist on hMPV infection were investigated in BALB/c mice.
|
33 |
24015257
|
Intranasal administration of the PAR1 agonist resulted in increased weight loss and mortality of infected mice.
|
34 |
24015257
|
Conversely, the PAR1 antagonist was beneficial to hMPV infection by decreasing weight loss and clinical signs and by significantly reducing pulmonary inflammation, pro-inflammatory cytokine levels (including IL-6, KC and MCP-1) and recruitment of immune cells to the lungs.
|
35 |
24015257
|
In addition, a significant reduction in pulmonary viral titers was also observed in the lungs of PAR1 antagonist-treated mice.
|
36 |
24015257
|
Despite no apparent direct effect on virus replication during in vitro experiments, an important role for PAR1 in the regulation of furin expression in the lungs was shown for the first time.
|
37 |
24015257
|
Further experiments indicated that the hMPV fusion protein can be cleaved by furin thus suggesting that PAR1 could have an effect on viral infectivity in addition to its immunomodulatory properties.
|
38 |
24015257
|
Thus, inhibition of PAR1 by selected antagonists could represent an interesting strategy for decreasing the severity of paramyxovirus infections.
|
39 |
24015257
|
Herein, the effects of a PAR1 agonist and a PAR1 antagonist on hMPV infection were investigated in BALB/c mice.
|
40 |
24015257
|
Intranasal administration of the PAR1 agonist resulted in increased weight loss and mortality of infected mice.
|
41 |
24015257
|
Conversely, the PAR1 antagonist was beneficial to hMPV infection by decreasing weight loss and clinical signs and by significantly reducing pulmonary inflammation, pro-inflammatory cytokine levels (including IL-6, KC and MCP-1) and recruitment of immune cells to the lungs.
|
42 |
24015257
|
In addition, a significant reduction in pulmonary viral titers was also observed in the lungs of PAR1 antagonist-treated mice.
|
43 |
24015257
|
Despite no apparent direct effect on virus replication during in vitro experiments, an important role for PAR1 in the regulation of furin expression in the lungs was shown for the first time.
|
44 |
24015257
|
Further experiments indicated that the hMPV fusion protein can be cleaved by furin thus suggesting that PAR1 could have an effect on viral infectivity in addition to its immunomodulatory properties.
|
45 |
24015257
|
Thus, inhibition of PAR1 by selected antagonists could represent an interesting strategy for decreasing the severity of paramyxovirus infections.
|
46 |
24015257
|
Herein, the effects of a PAR1 agonist and a PAR1 antagonist on hMPV infection were investigated in BALB/c mice.
|
47 |
24015257
|
Intranasal administration of the PAR1 agonist resulted in increased weight loss and mortality of infected mice.
|
48 |
24015257
|
Conversely, the PAR1 antagonist was beneficial to hMPV infection by decreasing weight loss and clinical signs and by significantly reducing pulmonary inflammation, pro-inflammatory cytokine levels (including IL-6, KC and MCP-1) and recruitment of immune cells to the lungs.
|
49 |
24015257
|
In addition, a significant reduction in pulmonary viral titers was also observed in the lungs of PAR1 antagonist-treated mice.
|
50 |
24015257
|
Despite no apparent direct effect on virus replication during in vitro experiments, an important role for PAR1 in the regulation of furin expression in the lungs was shown for the first time.
|
51 |
24015257
|
Further experiments indicated that the hMPV fusion protein can be cleaved by furin thus suggesting that PAR1 could have an effect on viral infectivity in addition to its immunomodulatory properties.
|
52 |
24015257
|
Thus, inhibition of PAR1 by selected antagonists could represent an interesting strategy for decreasing the severity of paramyxovirus infections.
|
53 |
24866378
|
Protease-activated receptor 1 suppresses Helicobacter pylori gastritis via the inhibition of macrophage cytokine secretion and interferon regulatory factor 5.
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54 |
24866378
|
Although protease-activated receptor 1 (PAR1) has been identified as one such host factor, its mechanism of action is unknown.
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55 |
24866378
|
Using chimeric mice, we demonstrated that PAR1-mediated protection against H. pylori gastritis requires bone marrow-derived cells.
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56 |
24866378
|
Analyses of the gastric mucosa revealed that PAR1 suppresses cellular infiltration and both T helper type 1 (Th1) and T helper type 17 (Th17) responses to infection.
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57 |
24866378
|
Moreover, PAR1 expression was associated with reduced vaccine-mediated protection against H. pylori.
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58 |
24866378
|
Analyses of H. pylori-stimulated macrophages revealed that PAR1 activation suppressed secretion of interleukin (IL)-12 and IL-23, key drivers of Th1 and Th17 immunity, respectively.
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59 |
24866378
|
Furthermore, PAR1 suppressed interferon regulatory factor 5 (IRF5), an important transcription factor for IL-12 and IL-23, both in the infected mucosa and following bacterial stimulation.
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60 |
24866378
|
PAR1 suppression of IRF5 and IL-12/23 secretion by macrophages provides a novel mechanism by which the host suppresses the mucosal Th1 and Th17 response to H. pylori infection.
|
61 |
24866378
|
Protease-activated receptor 1 suppresses Helicobacter pylori gastritis via the inhibition of macrophage cytokine secretion and interferon regulatory factor 5.
|
62 |
24866378
|
Although protease-activated receptor 1 (PAR1) has been identified as one such host factor, its mechanism of action is unknown.
|
63 |
24866378
|
Using chimeric mice, we demonstrated that PAR1-mediated protection against H. pylori gastritis requires bone marrow-derived cells.
|
64 |
24866378
|
Analyses of the gastric mucosa revealed that PAR1 suppresses cellular infiltration and both T helper type 1 (Th1) and T helper type 17 (Th17) responses to infection.
|
65 |
24866378
|
Moreover, PAR1 expression was associated with reduced vaccine-mediated protection against H. pylori.
|
66 |
24866378
|
Analyses of H. pylori-stimulated macrophages revealed that PAR1 activation suppressed secretion of interleukin (IL)-12 and IL-23, key drivers of Th1 and Th17 immunity, respectively.
|
67 |
24866378
|
Furthermore, PAR1 suppressed interferon regulatory factor 5 (IRF5), an important transcription factor for IL-12 and IL-23, both in the infected mucosa and following bacterial stimulation.
|
68 |
24866378
|
PAR1 suppression of IRF5 and IL-12/23 secretion by macrophages provides a novel mechanism by which the host suppresses the mucosal Th1 and Th17 response to H. pylori infection.
|
69 |
24866378
|
Protease-activated receptor 1 suppresses Helicobacter pylori gastritis via the inhibition of macrophage cytokine secretion and interferon regulatory factor 5.
|
70 |
24866378
|
Although protease-activated receptor 1 (PAR1) has been identified as one such host factor, its mechanism of action is unknown.
|
71 |
24866378
|
Using chimeric mice, we demonstrated that PAR1-mediated protection against H. pylori gastritis requires bone marrow-derived cells.
|
72 |
24866378
|
Analyses of the gastric mucosa revealed that PAR1 suppresses cellular infiltration and both T helper type 1 (Th1) and T helper type 17 (Th17) responses to infection.
|
73 |
24866378
|
Moreover, PAR1 expression was associated with reduced vaccine-mediated protection against H. pylori.
|
74 |
24866378
|
Analyses of H. pylori-stimulated macrophages revealed that PAR1 activation suppressed secretion of interleukin (IL)-12 and IL-23, key drivers of Th1 and Th17 immunity, respectively.
|
75 |
24866378
|
Furthermore, PAR1 suppressed interferon regulatory factor 5 (IRF5), an important transcription factor for IL-12 and IL-23, both in the infected mucosa and following bacterial stimulation.
|
76 |
24866378
|
PAR1 suppression of IRF5 and IL-12/23 secretion by macrophages provides a novel mechanism by which the host suppresses the mucosal Th1 and Th17 response to H. pylori infection.
|
77 |
24866378
|
Protease-activated receptor 1 suppresses Helicobacter pylori gastritis via the inhibition of macrophage cytokine secretion and interferon regulatory factor 5.
|
78 |
24866378
|
Although protease-activated receptor 1 (PAR1) has been identified as one such host factor, its mechanism of action is unknown.
|
79 |
24866378
|
Using chimeric mice, we demonstrated that PAR1-mediated protection against H. pylori gastritis requires bone marrow-derived cells.
|
80 |
24866378
|
Analyses of the gastric mucosa revealed that PAR1 suppresses cellular infiltration and both T helper type 1 (Th1) and T helper type 17 (Th17) responses to infection.
|
81 |
24866378
|
Moreover, PAR1 expression was associated with reduced vaccine-mediated protection against H. pylori.
|
82 |
24866378
|
Analyses of H. pylori-stimulated macrophages revealed that PAR1 activation suppressed secretion of interleukin (IL)-12 and IL-23, key drivers of Th1 and Th17 immunity, respectively.
|
83 |
24866378
|
Furthermore, PAR1 suppressed interferon regulatory factor 5 (IRF5), an important transcription factor for IL-12 and IL-23, both in the infected mucosa and following bacterial stimulation.
|
84 |
24866378
|
PAR1 suppression of IRF5 and IL-12/23 secretion by macrophages provides a novel mechanism by which the host suppresses the mucosal Th1 and Th17 response to H. pylori infection.
|
85 |
24866378
|
Protease-activated receptor 1 suppresses Helicobacter pylori gastritis via the inhibition of macrophage cytokine secretion and interferon regulatory factor 5.
|
86 |
24866378
|
Although protease-activated receptor 1 (PAR1) has been identified as one such host factor, its mechanism of action is unknown.
|
87 |
24866378
|
Using chimeric mice, we demonstrated that PAR1-mediated protection against H. pylori gastritis requires bone marrow-derived cells.
|
88 |
24866378
|
Analyses of the gastric mucosa revealed that PAR1 suppresses cellular infiltration and both T helper type 1 (Th1) and T helper type 17 (Th17) responses to infection.
|
89 |
24866378
|
Moreover, PAR1 expression was associated with reduced vaccine-mediated protection against H. pylori.
|
90 |
24866378
|
Analyses of H. pylori-stimulated macrophages revealed that PAR1 activation suppressed secretion of interleukin (IL)-12 and IL-23, key drivers of Th1 and Th17 immunity, respectively.
|
91 |
24866378
|
Furthermore, PAR1 suppressed interferon regulatory factor 5 (IRF5), an important transcription factor for IL-12 and IL-23, both in the infected mucosa and following bacterial stimulation.
|
92 |
24866378
|
PAR1 suppression of IRF5 and IL-12/23 secretion by macrophages provides a novel mechanism by which the host suppresses the mucosal Th1 and Th17 response to H. pylori infection.
|
93 |
24866378
|
Protease-activated receptor 1 suppresses Helicobacter pylori gastritis via the inhibition of macrophage cytokine secretion and interferon regulatory factor 5.
|
94 |
24866378
|
Although protease-activated receptor 1 (PAR1) has been identified as one such host factor, its mechanism of action is unknown.
|
95 |
24866378
|
Using chimeric mice, we demonstrated that PAR1-mediated protection against H. pylori gastritis requires bone marrow-derived cells.
|
96 |
24866378
|
Analyses of the gastric mucosa revealed that PAR1 suppresses cellular infiltration and both T helper type 1 (Th1) and T helper type 17 (Th17) responses to infection.
|
97 |
24866378
|
Moreover, PAR1 expression was associated with reduced vaccine-mediated protection against H. pylori.
|
98 |
24866378
|
Analyses of H. pylori-stimulated macrophages revealed that PAR1 activation suppressed secretion of interleukin (IL)-12 and IL-23, key drivers of Th1 and Th17 immunity, respectively.
|
99 |
24866378
|
Furthermore, PAR1 suppressed interferon regulatory factor 5 (IRF5), an important transcription factor for IL-12 and IL-23, both in the infected mucosa and following bacterial stimulation.
|
100 |
24866378
|
PAR1 suppression of IRF5 and IL-12/23 secretion by macrophages provides a novel mechanism by which the host suppresses the mucosal Th1 and Th17 response to H. pylori infection.
|
101 |
24866378
|
Protease-activated receptor 1 suppresses Helicobacter pylori gastritis via the inhibition of macrophage cytokine secretion and interferon regulatory factor 5.
|
102 |
24866378
|
Although protease-activated receptor 1 (PAR1) has been identified as one such host factor, its mechanism of action is unknown.
|
103 |
24866378
|
Using chimeric mice, we demonstrated that PAR1-mediated protection against H. pylori gastritis requires bone marrow-derived cells.
|
104 |
24866378
|
Analyses of the gastric mucosa revealed that PAR1 suppresses cellular infiltration and both T helper type 1 (Th1) and T helper type 17 (Th17) responses to infection.
|
105 |
24866378
|
Moreover, PAR1 expression was associated with reduced vaccine-mediated protection against H. pylori.
|
106 |
24866378
|
Analyses of H. pylori-stimulated macrophages revealed that PAR1 activation suppressed secretion of interleukin (IL)-12 and IL-23, key drivers of Th1 and Th17 immunity, respectively.
|
107 |
24866378
|
Furthermore, PAR1 suppressed interferon regulatory factor 5 (IRF5), an important transcription factor for IL-12 and IL-23, both in the infected mucosa and following bacterial stimulation.
|
108 |
24866378
|
PAR1 suppression of IRF5 and IL-12/23 secretion by macrophages provides a novel mechanism by which the host suppresses the mucosal Th1 and Th17 response to H. pylori infection.
|