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

Abstract

Vibrio parahaemolyticus (Vp), a major food-borne pathogen, is responsible for severe infections such as gastroenteritis and septicemia, which may be accompanied by lifethreatening 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.

Probiotic Yeasts and Vibrio anguillarum Infection Modify the Microbiome of Zebrafish Larvae

“…This result suggests that larval survival could be predicted by the abundance of some key genera, rather than the modification of microbial diversity. Several authors show that infections can induce disturbances in the composition of commensal microbiota such as overgrowth of some microorganisms and reduction of others ( Khan and Chousalkar, 2020 ; Vakili et al, 2020 ; Wang et al, 2020 ). For example, V. anguillarum affected the relative abundance of 18 OTUs (Operational Taxonomic Units) and altered alpha and beta diversity ( Nie et al, 2017 ) in ayu ( Plecoglossus altivelis ).…”

Decreased Ecological Resistance of the Gut Microbiota in Response to Clindamycin Challenge in Mice Colonized with the Fungus Candida albicans

“…Factors that affect microbiota composition often have a strong effect and produce changes in composition that can be detected at the phylum level. For example, dietary changes ( 27 , 28 ) and colonization with diverse microbes (e.g., Cryptosporidium parvum [ 29 ], Vibrio parahaemolyticus [ 30 ], and Klebsiella pneumoniae [ 31 ]) produce phylum-level changes. In contrast, the compositions of uncolonized and C. albicans -colonized mice under the conditions of our experiments showed minimal differences at the phylum level ( Fig.…”

Modulation of Intestinal Barrier, Inflammatory Response, and Gut Microbiota by Pediococcus pentosaceus zy-B Alleviates Vibrio parahaemolyticus Infection in C57BL/6J Mice

“…Species with differential abundance between groups were identified based on LDA scores greater than 3.6. 11 The abundance of species in the phylum Bacteroidetes and the genus Bacteroides were enriched in the control group but not in the other groups. Due to the Vp infection, the gut microflora abundance of the phylum Proteobacteria, the genera Enterobacter, and Prevotella were enriched in the Vp group.…”

“…9,10 A previous study of ours showed that a lack of intestinal microbial protection signals promotes Vpinduced bleeding and fluid accumulation in the ileum, triggering a pro-inflammatory cascade in the intestinal lamina propria. 11 Thus, there are inextricable links between the Vp infection and intestinal microecology. We believe that promoting a healthy gut microbial community could be an effective treatment strategy for Vp infection.…”

“…Vp can adapt and survive in the host gastrointestinal tract (GIT) causing vomition, diarrhea, and acute gastroenteritis . Vp invades the intestinal barrier causing inflammatory damage via cytotoxicity induced by virulence factors including thermostable direct hemolysin (TDH), TDH-related hemolysin, and pathogenic extracellular enzymes. , A previous study of ours showed that a lack of intestinal microbial protection signals promotes Vp-induced bleeding and fluid accumulation in the ileum, triggering a pro-inflammatory cascade in the intestinal lamina propria . Thus, there are inextricable links between the Vp infection and intestinal microecology.…”