Vibrio parahaemolyticus Infection in Mice Reduces Protective Gut Microbiota, Augmenting Disease Pathways

Rundong Wang; Yijia Deng; Qi Deng; Dongfang Sun; Zhijia Fang; Lijun Sun; Yaling Wang; Ravi Gooneratne

doi:10.3389/fmicb.2020.00073

Vibrio parahaemolyticus Infection in Mice Reduces Protective Gut Microbiota, Augmenting Disease Pathways

Front Microbiol. 2020 Jan 30:11:73. doi: 10.3389/fmicb.2020.00073. eCollection 2020.

Authors

Rundong Wang^{1

2}, Yijia Deng¹, Qi Deng¹, Dongfang Sun¹, Zhijia Fang¹, Lijun Sun¹, Yaling Wang¹, Ravi Gooneratne³

Affiliations

¹ College of Food Science and Technology, Guangdong Ocean University, Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, Key Laboratory of Advanced Processing of Aquatic Products of Guangdong Higher Education Institution, Zhanjiang, China.
² School of Chemistry and Chemical Engineering, Key Laboratory of Clean Energy Materials Chemistry of Guangdong Higher Education Institutes, Lingnan Normal University, Zhanjiang, China.
³ Department of Wine, Food and Molecular Biosciences, Faculty of Agriculture and Life Sciences, Lincoln University, Lincoln, New Zealand.

Abstract

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-1β, IL-6, and TNF-α in normal mice were ∼2.5-fold higher than in the PGF mice, and liver (ALT, AST, ALP) and kidney (BUN) function indices were ∼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.

Keywords: 16S rRNA gene; Vibrio parahaemolyticus infection; gene sequencing; gut microbiota; pathogenesis.