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Effect of luxS encoding a synthase of quorum-sensing signal molecule AI-2 of Vibrio vulnificus on mouse gut microbiome

Authors
Lee, Keun-WooJie, HaneulKim, SoyeeBaek, Min-GyungYi, HanaKim, Kun-Soo
Issue Date
May-2022
Publisher
SPRINGER
Keywords
Vibrio vulnificus; Quorum-sensing; AI-2; Microbiome; Lactobacillus; Lactic acid
Citation
APPLIED MICROBIOLOGY AND BIOTECHNOLOGY, v.106, no.9-10, pp.3721 - 3734
Indexed
SCIE
SCOPUS
Journal Title
APPLIED MICROBIOLOGY AND BIOTECHNOLOGY
Volume
106
Number
9-10
Start Page
3721
End Page
3734
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/143072
DOI
10.1007/s00253-022-11935-w
ISSN
0175-7598
Abstract
Autoinducer-2 (AI-2), a quorum-sensing signal molecule from the human pathogen Vibrio vulnificus, was assessed for its effect on the gut microbiome of mice. For this, we employed 16S rRNA sequencing to compare the gut microbiome of mice infected with either wild-type V. vulnificus or with the isotype Delta luxS that has a deletion in luxS which encodes the biosynthetic function of AI-2. The relative ratio of wild-type Vibrio species in the jejunum and ileum of mice infected with the wild type was significantly higher than that in mice infected with Delta luxS, suggesting that AI-2 plays an important role in the colonization of V. vulnificus in the small intestine. The bacterial composition in the gut of mice infected with Delta luxS comprises a higher proportion of Firmicutes, composed mainly of Lactobacillus, compared to the mice infected with wild-type cells. In the large intestine, Vibrio species were barely detected regardless of genetic background. Three Lactobacillus spp. isolated from fecal samples from mice infected with Delta luxS manifested significant antibacterial activities against V. vulnificus. Culture supernatants from these three species were dissolved by HPLC, and a substance in fractions showing inhibitory activity against V. vulnificus was determined to be lactic acid. Our results suggest that luxS in V. vulnificus affects not only the ability of the species to colonize the host gut but also its susceptibility to the growth-inhibiting activity of commensal bacteria including Lactobacillus.
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