文献类型：期刊文献

英文题名：Vibrio parahaemolyticus Infection in Mice Reduces Protective Gut Microbiota, Augmenting Disease Pathways

作者：Wang, Rundong[1,2];Deng, Yijia[1];Deng, Qi[1];Sun, Dongfang[1];Fang, Zhijia[1];Sun, Lijun[1];Wang, Yaling[1];Gooneratne, Ravi[3]

机构：[1]Guangdong Ocean Univ, Key Lab Adv Proc Aqut Prod, Coll Food Sci & Technol,Guangdong Higher Educ Ins, Guangdong Prov Key Lab Aquat Prod Proc & Safety, Zhanjiang, Peoples R China;[2]Lingnan Normal Univ, Sch Chem & Chem Engn, Key Lab Clean Energy Mat Chem, Guangdong Higher Educ Inst, Zhanjiang, Peoples R China;[3]Lincoln Univ, Fac Agr & Life Sci, Dept Wine Food & Mol Biosci, Lincoln, New Zealand

年份：2020

卷号：11

外文期刊名：FRONTIERS IN MICROBIOLOGY

收录：SCI-EXPANDED(收录号：WOS:000515366800001)、、WOS

基金：This research was supported by grants from the National Science Foundation (No. 31371746) and the Guangdong Provincial Special Fund for Technological Innovation of Modern Agricultural Industry (No. 2019KJ151).

语种：英文

外文关键词：pathogenesis; Vibrio parahaemolyticus infection; gut microbiota; 16S rRNA gene; gene sequencing

外文摘要：Vibrio parahaemolyticus (Vp), a major food-borne pathogen, is responsible for severe infections such as gastroenteritis and septicemia, which may be accompanied by life-threatening complications. While studies have evaluated factors that affect the virulence of the pathogen, none have investigated the interaction of Vp with gut microbiota. To address this knowledge gap, we compared the effect of Vp on gut bacterial community structure, immunity, liver and kidney function, in pseudo germ-free (PGF) mice and normal (control) mice. Significant damage to the ileum was observed in normal mice compared with the PGF mice. The inflammatory factors IL-1 beta, IL-6, and TNF-alpha in normal mice were similar to 2.5-fold higher than in the PGF mice, and liver (ALT, AST, ALP) and kidney (BUN) function indices were similar to 1.6-fold higher. The Vp infection substantially reduced species composition and richness of the gut microbial communities. In particular, there was a shift in keystone taxa, from protective species of genera Bacteroides, Lactobacillus, Bifidobacterium, and Akkermansia in the gut of control mice to opportunistic pathogens Enterobacteriaceae, Proteus, Prevotella, and Sutterella in Vp-infected mice, thus affecting microbiota-related biological functions in the mice. Specifically, pathways involved in infectious diseases and ion channels were significantly augmented in infected mice, while the pathways involved in metabolism, digestion and cell growth declined. We propose that the normal mice are more prone to Vp infection because of the alteration in gut-microbe-mediated functions. All these effects reduce intestinal resistance, with marked damage to the gut lining and pathogen leakage into the blood culminating in liver and kidney damage. These findings greatly advance our understanding of the mechanisms underlying interactions between Vp, the gut microbiota and the infected host.