{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T07:48:27Z","timestamp":1791186507043,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2014,3,20]],"date-time":"2014-03-20T00:00:00Z","timestamp":1395273600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"NIH","award":["AI0698142"],"award-info":[{"award-number":["AI0698142"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Gastro and Hepatol"],"published-print":{"date-parts":[[2014,4]]},"abstract":"Abstract<\/jats:title>Background and Aim<\/jats:title>Hepatocyte growth factor (HGF<\/jats:styled-content>) is a pleiotropic cytokine related with cell proliferation and survival; however, its role in viral hepatitis is not elucidated. In this study, we studied HGF<\/jats:styled-content> immune role in viral hepatitis.<\/jats:p><\/jats:sec>Methods<\/jats:title>Mice received hydrodynamically delivered HGF<\/jats:styled-content> plasmid or control plasmid and then infected with adenovirus, and parameters of immune\u2010mediated liver damage were evaluated. We studied dendritic cell (DC<\/jats:styled-content>) activation in the presence of HGF<\/jats:styled-content>. T<\/jats:styled-content> cells collected from infected mice were restimulated with virally infected DC<\/jats:styled-content> to measure cytokine production in vitro<\/jats:italic>.<\/jats:p><\/jats:sec>Results<\/jats:title>HGF<\/jats:styled-content> ameliorated the liver inflammation during viral hepatitis as alanine transferase, intrahepatic lymphocytes, and splenocyte counts were diminished by HGF<\/jats:styled-content>. Lower histological scores of liver pathology were observed in the HGF<\/jats:styled-content> group. DC<\/jats:styled-content> from the HGF<\/jats:styled-content> group expressed reduced C<\/jats:styled-content>D<\/jats:styled-content>40. The hepatic expression and serum concentration of IL<\/jats:styled-content>\u201012p40 were diminished in HGF<\/jats:styled-content>\u2010transfected mice. In vitro<\/jats:italic> experiments with DC<\/jats:styled-content> confirmed that HGF<\/jats:styled-content> diminished CD<\/jats:styled-content>40 expression and IL<\/jats:styled-content>\u201012p40 production. The expression and serum levels of IFN<\/jats:styled-content>\u2010\u03b3, IL<\/jats:styled-content>\u20106 and CXCL<\/jats:styled-content>9 were significantly decreased in the HGF<\/jats:styled-content> group. HGF<\/jats:styled-content> overexpression diminished the expression and concentration of IL<\/jats:styled-content>\u201010 and TGF<\/jats:styled-content>\u2010\u03b2. The frequency of PD<\/jats:styled-content>\u20101+<\/jats:sup>T<\/jats:styled-content>im\u20103+<\/jats:sup> in CD<\/jats:styled-content>8 T<\/jats:styled-content> cells was decreased by HGF<\/jats:styled-content> overexpression. Moreover, T<\/jats:styled-content> cells in the HGF<\/jats:styled-content> group at day 14 secreted more IFN<\/jats:styled-content>\u2010\u03b3 and TNF<\/jats:styled-content>\u2010\u03b1 than those in the control group when restimulated with virally infected DC<\/jats:styled-content>.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>HGF<\/jats:styled-content> modulated DC<\/jats:styled-content> activation and T<\/jats:styled-content> cell priming, thereby limiting the immune\u2010mediated damage in the liver. However, viral clearance was not compromised by HGF<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jgh.12456","type":"journal-article","created":{"date-parts":[[2013,11,14]],"date-time":"2013-11-14T02:50:52Z","timestamp":1384397452000},"page":"878-886","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Hepatocyte growth factor in dampening liver immune\u2010mediated pathology in acute viral hepatitis without compromising antiviral activity"],"prefix":"10.1111","volume":"29","author":[{"given":"Renan","family":"Aguilar\u2010Valenzuela","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology The University of Texas Medical Branch Galveston Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric D.","family":"Carlsen","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology The University of Texas Medical Branch 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