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Toll like receptor 2 knock‐out attenuates carbon tetrachloride (CCl 4 )‐induced liver fibrosis by downregulating MAPK and NF‐κB signaling pathways
Author(s) -
Ji Lingling,
Xue Ruyi,
Tang Wenqing,
Wu Weibin,
Hu Tingting,
Liu Xijun,
Peng Xiaomin,
Gu Jianxin,
Chen She,
Zhang Si
Publication year - 2014
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2014.04.042
Subject(s) - tlr2 , proinflammatory cytokine , chemistry , mapk/erk pathway , signal transduction , toll like receptor , liver injury , hepatic stellate cell , fibrosis , nf κb , p38 mitogen activated protein kinases , cancer research , receptor , microbiology and biotechnology , tlr4 , innate immune system , inflammation , endocrinology , medicine , immunology , biology , biochemistry
Innate immune signaling associated with Toll‐like receptors (TLRs) is a key pathway involved in the progression of liver fibrosis. In this study, we reported that TLR2 is required for hepatic fibrogenesis induced by carbon tetrachloride (CCl 4 ). After CCl 4 treatment, TLR2 −/− mice had reduced liver enzyme levels, diminished collagen deposition, decreased inflammatory infiltration and impaired activation of hepatic stellate cells (HSCs) than wild type (WT) mice. Furthermore, after CCl 4 treatment, TLR2 −/− mice demonstrated downregulated expression of profibrotic and proinflammatory genes and impaired mitogen‐activated protein kinases (MAPK) and nuclear factor kappa B (NF‐κB) activation than WT mice. Collectively, our data indicate that TLR2 deficiency protects against CCl 4 ‐induced liver fibrosis.