2008
DOI: 10.1164/rccm.200708-1184oc
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Exacerbation of Established Pulmonary Fibrosis in a Murine Model by Gammaherpesvirus

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Cited by 100 publications
(115 citation statements)
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“…MCP-1 has previously been reported to be a major profibrotic chemokine involved in various fibrotic processes, including recruitment of fibrocytes, induction of collagen synthesis, and up-regulation of TGF-␤1 expression in various models. 50,51,[55][56][57][58][59][60][61][63][64][65][66][67][68] Indeed, we observed that MCP-1 responses preceded the responses of fibrogenic growth factor TGF-␤1, 51,52 which were significantly higher in the lung of infected TNF Ϫ/Ϫ lungs and were well correlated with fibrotic tissue remodeling seen in TNF Ϫ/Ϫ lungs at later time points during influenza infection. Thus, depletion of MCP-1 in influenza-infected TNF Ϫ/Ϫ hosts markedly reduced lung immunopathology and tissue remodeling, and such MCP-1 depletion-improved welfare was associated with diminished production of bioactive TGF-␤1.…”
Section: Discussionmentioning
confidence: 84%
See 1 more Smart Citation
“…MCP-1 has previously been reported to be a major profibrotic chemokine involved in various fibrotic processes, including recruitment of fibrocytes, induction of collagen synthesis, and up-regulation of TGF-␤1 expression in various models. 50,51,[55][56][57][58][59][60][61][63][64][65][66][67][68] Indeed, we observed that MCP-1 responses preceded the responses of fibrogenic growth factor TGF-␤1, 51,52 which were significantly higher in the lung of infected TNF Ϫ/Ϫ lungs and were well correlated with fibrotic tissue remodeling seen in TNF Ϫ/Ϫ lungs at later time points during influenza infection. Thus, depletion of MCP-1 in influenza-infected TNF Ϫ/Ϫ hosts markedly reduced lung immunopathology and tissue remodeling, and such MCP-1 depletion-improved welfare was associated with diminished production of bioactive TGF-␤1.…”
Section: Discussionmentioning
confidence: 84%
“…Compelling evidence suggests that MCP-1 is not only a chemokine for mononuclear cells, but of importance, it is also a profibrotic cytokine capable of direct up-regulation of TGF-␤1 expression [55][56][57][58][59][60][61] and recruitment and induction of collagen synthesis by fibrocytes. 51,[62][63][64][65][66][67][68] Thus, given the dysregulated MCP-1 and its association with heightened TGF-␤1 production seen in influenza-infected TNF Ϫ/Ϫ lungs (Figure 7), we further investigated the role of MCP-1 in heightened immunopathology and fibrotic reaction in the lung of TNF Ϫ/Ϫ mice by means of MCP-1 depletion.…”
Section: Attenuation Of Lung Immunopathology In Influenza-infected Tnmentioning
confidence: 99%
“…In animal models there is now good evidence to show that viral infection can exacerbate established fibrosis and in so doing gives rise to a lesion resembling DAD [37]. However, in a study of 43 individuals suffering an acute exacerbation of IPF, WOOTTON et al [13] failed to clearly identify a viral or other infectious trigger for the acute exacerbation in the vast majority of their subjects.…”
Section: Infection and Acute Exacerbations Of Ipfmentioning
confidence: 99%
“…Despite this, the lungs of FITC-treated mice infected 14 or 21 days previously with gHV-68 (solid bars) displayed a significant augmentation in collagen levels compared with mock-infected mice treated with FITC (n 5 3-11 per group). latent infection caused a persistent increase in CCL2 and CCL12 protein production (11,24,25). We infected mice intranasally with 5 3 10 4 PFU gHV-68 on Day 0, and the lungs of the infected mice were harvested 15, 24, and 38 d.p.i.…”
Section: Ccl2 and Ccl12 Levels Are Increased In The Lungs Beyond The mentioning
confidence: 99%
“…In addition, we have recently shown that lytic gHV-68 infection can exacerbate established pulmonary fibrosis (11). The mechanisms identified to contribute to lytic virus-induced exacerbation of fibrosis have included Th2 bias, persistent reactivation, alternative activation of macrophages, and fibrocyte recruitment (11)(12)(13).…”
mentioning
confidence: 99%