Enterobacter cloacae aggravates metabolic disease by inducing inflammation and lipid accumulation
Enterobacter cloacae aggravates metabolic disease by inducing inflammation and lipid accumulation
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阴沟肠杆菌通过诱导炎症和脂质积累加重代谢疾病
DOI：
10.1016/j.etap.2022.103819
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发表时间：
2022-01-25
影响因子：
4.3
通讯作者：
Feng, Haihua
中科院分区：
文献类型：
--
作者：
Jin, Meiyu;Zheng, Lianwen;Feng, Haihua
众所周知，肠道微生物群失衡可促进代谢性疾病的发展。阴沟肠杆菌（Enterobacter cloylum，E.大肠杆菌是一种肠道条件致病菌。因此，我们假设E.氯吡格雷加速了代谢性疾病的发展。为了回答这个问题，我们使用了E。Cloacetate诱发豚鼠疾病。采用H&E染色法观察肝脏和主动脉的病理变化，油红O染色法观察肝脏脂质沉积情况。我们使用试剂盒检测AST含量，并使用Western blot检测肝脏中的蛋白质水平。我们发现E.氯吡格雷可引起豚鼠肝脏病理改变、脂质蓄积及主动脉壁病理改变。和E.氯吡格雷使肝指数升高5.94%，血清AST升高41.93U/L。重要的是，E。氯吡格雷激活肝高迁移率族蛋白（HMGB 1）/Toll样受体4（TLR 4）/髓样分化因子88（MYD 88）/核因子κ B（NF-κ B）信号和固醇调节元件结合蛋白1c（SREBP-1c），抑制AMP激活的蛋白激酶（AMPK）。我们的结论是E. Clobacillus通过诱导炎症和脂质积累促进非酒精性脂肪性肝病（NAFLD），而E.氯吡格雷还促进动脉粥样硬化。这些发现对NAFLD和动脉粥样硬化的发病机制和药物筛选研究具有重要意义。
It is well known that gut microbiota imbalance can promote the development of metabolic disease. Enterobacter cloacae (E. cloacae) is a kind of opportunistic pathogen in the intestine. Therefore, we hypothesized that E. cloacae accelerated the development of metabolic disease. To answer this question, we used E. cloacae to induce disease in guinea pigs. We used H&E staining to detect the pathological changes of liver and aorta and used Oil Red O staining to evaluate the lipid accumulation in the liver. And that we used a kit to detect AST content and used Western blot to detect protein levels in the liver. We found that E. cloacae could induce liver pathological changes and lipid accumulation as well as aortic wall pathological changes in guinea pigs. And E. cloacae increased the liver index to 5.94% and the serum AST level to 41.93 U/L. Importantly, E. cloacae activated liver high mobility group protein (HMGB1)/toll-like receptor 4 (TLR4)/myeloiddifferentiationfactor88 (MYD88)/nuclear factor kappa B (NF-kappa B) signal and sterol regulatory element-binding protein 1c (SREBP-1c) and inhibited AMP activated protein kinase (AMPK). We conclude that E. cloacae promote nonalcoholic fatty liver disease (NAFLD) by inducing inflammation and lipid accumulation, and E. cloacae also promote atherosclerosis. These findings are important for study on the pathogenesis and drug screening of NAFLD and atherosclerosis.