Abstract
BackgroundA foodborne pathogen, Vibrio vulnificus, encounters normal microflora inhabiting the gut environments prior to causing fatal septicemia or gastroenteritis and should overcome the barriers derived from the gut commensals for successful infection. Its interactions with gut commensals during the infection process, however, have not yet been understood. In the present study, the effect of V. vulnificus on the community structures of gut microbiota in mice was examined.ResultsAnalyses of microbiota in the fecal samples of mice that died due to V. vulnificus infection revealed the decreased abundance of bacteria belonged to Bacteroidetes, notably, the species Bacteroides vulgatus. In vitro coculturing of the two bacterial species resulted in the decreased survival of B. vulgatus. The antagonistic effect of V. vulnificus against B. vulgatus was found to be mediated by cyclo-Phe-Pro (cFP), one of the major compounds secreted by V. vulnificus. cFP-treated B. vulgatus showed collapsed cellular morphology with an undulated cell surface, enlarged periplasmic space, and lysed membranes, suggesting the occurrence of membrane disruption. The degree of membrane disruption caused by cFP was dependent upon the cellular levels of ObgE in B. vulgatus. Recombinant ObgE exhibited a high affinity to cFP at a 1:1 ratio. When mice were orally injected with cFP, their feces contained significantly reduced B. vulgatus levels, and their susceptibility to V. vulnificus infection was considerably increased.ConclusionsThis study demonstrates that V. vulnificus-derived cFP modulates the abundance of the predominant species among gut commensals, which made V. vulnificus increase its pathogenicity in the hosts.2SB4iqYCk6h9vi_xizs4mWVideo abstract
Highlights
During the infection processes of foodborne pathogens, they encounter numerous stresses through the gastrointestinal (GI) tract of the host
Reduced levels of B. vulgatus in the fecal microbiota of the V. vulnificus-infected mice Fecal samples were collected from mice, which had been subjected to gavage with V. vulnificus and died within 20 h post-infection
Analysis of 16S rDNA sequences amplified from the prokaryotic cells of the domain Bacteria in fecal samples showed that Bacteroidetes and Firmicutes were the major phyla occupying approximately 53% and 40% of total fecal microbiomes in the control mice, respectively (Fig. 1A)
Summary
During the infection processes of foodborne pathogens, they encounter numerous stresses through the gastrointestinal (GI) tract of the host. Kim et al Microbiome (2021) 9:161 lipoprotein A (IlpA), hemolysin/cytolysin (VvhA), metalloprotease M (VvpM), phospholipase A2 (PlpA), and multifunctional-autoprocessing repeats-in-toxin (MARTX) show diverse activities to cause immunogenicity, cytotoxicity, and cell death via necrosis or apoptosis [8, 9]. Production of these virulence factors is strictly regulated by sensing the extracellular signals derived from hosts or bacteria to express them in appropriate conditions. A foodborne pathogen, Vibrio vulnificus, encounters normal microflora inhabiting the gut environments prior to causing fatal septicemia or gastroenteritis and should overcome the barriers derived from the gut commensals for successful infection. The effect of V. vulnificus on the community structures of gut microbiota in mice was examined
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