Toll like receptor 2 knock-out attenuates carbon tetrachloride (CC14)-induced liver fibrosis by downregulating MAPK and NF-κB signaling pathways

作者：Ji, Lingling; Xue, Ruyi; Tang, Wenqing; Wu, Weibin; Hu, Tingting; Liu, Xijun; Peng, Xiaomin; Gu, Jianxin; Chen, She^*; Zhang, Si

来源：FEBS LETTERS, 2014, 588(12): 2095-2100.

DOI：10.1016/j.febslet.2014.04.042

• Liver fibrosis
• Toll like receptor 2
• Carbon tetrachloride
• Hepatic stellate cell
• mitogen-activated protein kinases
• NF-kappa B

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 (CCl4). After CCl4 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 CCl4 treatment, TLR2(-/-) mice demonstrated downregulated expression of profibrotic and proinflammatory genes and impaired nitogen-activated protein kinases (MAPK) and nuclear factor kappa B (NF-kappa B) activation than WT mice. Collectively, our data indicate that TLR2 deficiency protects against CCl4-induced liver fibrosis.

• 出版日期2014-6-5
• 单位复旦大学