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Fielding, Ceri A.; Jones, Gareth W.; McLoughlin, Rachel M.; McLeod, Louise; Hammond, Victoria J.; Uceda, Javier; Williams, Anwen S.; Lambie, Mark; Foster, Thomas L.; Liao, Chia-Te; Rice, Christopher M.; Greenhill, Claire J.; Colmont, Chantal S.; Hams, Emily; Coles, Barbara; Kift-Morgan, Ann; Newton, Zarabeth; Craig, Katherine J.; Williams, John D.; Williams, Geraint T.; Davies, Simon J.; Humphreys, Ian R.; O’Donnell, Valerie B.; Taylor, Philip R.; Jenkins, Brendan J.; Topley, Nicholas; Jones, Simon A.
Immunity (Cambridge, Mass.), 01/2014, Letnik: 40, Številka: 1Journal Article
Fibrosis in response to tissue damage or persistent inflammation is a pathological hallmark of many chronic degenerative diseases. By using a model of acute peritoneal inflammation, we have examined how repeated inflammatory activation promotes fibrotic tissue injury. In this context, fibrosis was strictly dependent on interleukin-6 (IL-6). Repeat inflammation induced IL-6-mediated T helper 1 (Th1) cell effector commitment and the emergence of STAT1 (signal transducer and activator of transcription-1) activity within the peritoneal membrane. Fibrosis was not observed in mice lacking interferon-γ (IFN-γ), STAT1, or RAG-1. Here, IFN-γ and STAT1 signaling disrupted the turnover of extracellular matrix by metalloproteases. Whereas IL-6-deficient mice resisted fibrosis, transfer of polarized Th1 cells or inhibition of MMP activity reversed this outcome. Thus, IL-6 causes compromised tissue repair by shifting acute inflammation into a more chronic profibrotic state through induction of Th1 cell responses as a consequence of recurrent inflammation. •Repeated acute resolving inflammation leads to excessive tissue damage•IL-6 regulates profibrotic IFN-γ-secreting T cells•IFN-γ increases detrimental STAT1 signaling in stromal tissue•STAT1 activity alters homeostatic control of extracellular matrix to promote fibrosis
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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