LPS Inhibits Fatty Acid Absorption in Enterocytes through TNF-α Secreted by Macrophages

作者: Heyuan Liu , Lixia Kai , Huahua Du , Xinxia Wang , Yizhen Wang

DOI: 10.3390/CELLS8121626

关键词:

摘要: Diarrhea, such as steatorrhea, could result from fat absorption disorders, which be caused by many factors, including Escherichia coli infection. However, it is not clear how E. affects fatty acid in animals. Lipopolysaccharide (LPS), one of the main pathogenic components coli, cause virulence coli. Therefore, we used LPS to explore underlying mechanism that causes inhibition intestine. In this study, found apoptosis intestinal epithelial cells mice. Further, caspase-3 activation porcine enterocyte cell line (IPEC-J2). direct treatment did induce any significant change IPEC-J2. We then prepared conditioned medium LPS-treated macrophage (3D4/2) for incubating IPEC-J2, initiates inflammation activating immune cells. The decreased and While inhibiting no longer serious deficiency absorption. As IL-1β, IL-6, TNF-α increase significantly, IPEC-J2 was treated with TNF-α, respectively. Only induced Reducing secretion 3D4/2, there obvious recovered effectively. Based on above results, hold opinion does suppress directly intestine, but may work macrophages secrete cytokines, inducing finally leading

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