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Hepatic microenvironment underlies fibrosis in chronic hepatitis B patients

World Journal of Gastroenterology 2020年第27期26卷 3917-3928页

作者： Qun-Yan Yao Ya-Dong Feng Pei Han Feng Yang Guang-Qi Song Department of Gastroenterology and Hepatology Zhongshan HospitalFudan UniversityShanghai 201332China Shanghai Institute of Liver Diseases Shanghai 201332China Otsuka Shanghai Research Institute Shanghai 201318China Department of Pancreatic Surgery Pancreatic Disease InstituteHuashan HospitalShanghai Medical CollegeFudan UniversityShanghai 200040China

BACKGROUND Chronic hepatitis B virus(HBV)infection is a leading cause of liver morbidity and mortality *** fibrosis resulting from viral infection-associated inflammation and direct liver damage plays an important role in disease management and *** mechanisms underlying the contribution of the liver microenvironment to fibrosis in HBV patients are not fully *** is an absence of effective clinical treatments for liver fibrosis progression;thus,establishing a suitable in vitro microenvironment in order to design novel therapeutics and identify molecular biomarkers to stratify patients is urgently *** To examine a subset of pre-selected microenvironment factors of chronic HBV patients that may underlie fibrosis,with a focus on fibroblast *** We examined the gene expression of key microenvironment factors in liver samples from patients with more advanced fibrosis compared with those with less severe *** also used the human stellate cell line LX-2 in the in vitro *** different recombinant cytokines and growth factors or their combination,we studied how these factors interacted with LX-2 cells and pinpointed the crosstalk between the aforementioned factors and screened the most important *** Of the secreted factors examined,transforming growth factor(TGF)-β1,interleukin(IL)-1βand tumor necrosis factor(TNF)-αwere increased in patients with advanced *** found that besides TGF-β1,IL-1βcan also induce a profibrotic cascade by stimulating the expression of connective tissue growth factor and platelet-derived growth factor(PDGF)in LX-2 ***,the proinflammatory response can be elicited in LX-2 cells following treatment with IL-1βand TNF-α,suggesting that stellate cells can respond to proinflammatory *** combining IL-1βand TGF-β1,we observed not only fibroblast activation as shown byαlpha-smooth muscle actin and PDGF induction,but also the inflammatory response

关键词： Microenvironment Liver fibrosis Chronic hepatitis B human stellate cell Interleukin-1β

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