Lactobacillus alleviates intestinal epithelial barrier function through GPR43-mediated M2 macrophage polarization  

作　　者：Yong Yao Yuhan Zhang Mengzhen Song Jinping Fan Shengkai Feng Jingjing Li Zhifeng Wu Bo Zuo Shiyu Tao Xiangdong Liu 

机构地区：[1]College of Animal Sciences and Technology,Huazhong Agricultural University,Wuhan 430070,China

出　　处：《Animal Diseases》2025年第1期56-72,共17页动物疾病(英文)

基　　金：supported by the National Nature Science Foundation of China(32272898);the National Key Research and Development Program(2021YFA0805904);the Fundamental Research Funds for the Central Universities(2662020DKQD004).

摘　　要：Lactobacillus species have excellent abilities to reduce intestinal inflammation and enhance gut barrier function.This study elucidated the potential mechanisms through which Lactobacillus mitigates lipopolysaccharide(LPS)-induced intestinal injury from the perspective of macrophage-intestinal epithelial cell interactions.Lactobacillus intervention improved the histopathological score;elevated ZO-1 and Occludin protein production;reduced CD16^(+)cell numbers;diminished IL-1β,IL-6,and TNF-αlevels;decreased inducible nitric oxide synthase(iNOS)expression;increased CD163^(+)cell numbers;elevated IL-10 concentration;and increased arginase-1(Arg1)expression in LPS-challenged piglets.Lactobacillus pretreatment also altered the colonic microbiota,thereby increasing the butyric acid concentration and GPR43 expression in the LPS-challenged piglets.Compared with those in the LPS group,sodium butyrate(SB)pretreatment decreased IL-1β,IL-6 and TNF-αsecretion and iNOS expression but increased IL-10 secretion and Arg1 expression in macrophages.The SB-pretreated macrophages reduced the protein expression of TLR4,MyD88,and phosphorylated NF-κB p65 but increased the protein expression of ZO-1 and Occludin in intestinal epithelial cells.Moreover,GLPG0974 blocked the beneficial effects of SB on macrophages and intestinal epithelial cells.This study demonstrated that Lactobacillus improves intestinal barrier function by regulating the macrophage phenotype through the control of butyric acid and GPR43 levels to further control inflammation.

关 键 词：LACTOBACILLUS Butyric acid GPR43 MACROPHAGE Gut barrier 

分 类 号：R73[医药卫生—肿瘤]