Investigation of pathogenesis of NAFLD in disturbance of hepatic and intestinal Toll-like receptor signal and alternation of microbiota

本研究探讨了高脂饮食小鼠肠-肝轴中TLRs的表达。TLRs的表达在无炎症的NAFLD肝脏中已经上调，但在小肠中下调。抗生素治疗改善了肝脏中的脂肪变性和TLR表达。脂肪酸上调库普弗细胞和肝细胞模型中的TLR表达。在NAFLD的促炎状态的发展中，脂肪酸触发TLR的表达，这有助于通过肠道微生物群的TLR信号诱导炎性细胞因子。

In this study, we investigated the expression of TLRs in gut-liver axis in high fat fed mice. The expression of TLRs was already upregulated in NAFLD liver without inflammation, but downregulated in small intestine. Antibiotics treatment improved steatosis and TLR expression in the liver. Fatty acids upregulated TLRs expression in Kupffer cell and hepatocyte models. In the development of the pro-inflammatory state of NAFLD, fatty acids trigger the expressions of TLRs, which contribute to the induction of inflammatory cytokines through TLR signals by the intestinal microbiota.