The Bactericidal Lectin RegIIIβ Prolongs Gut Colonization and
Enteropathy in the Streptomycin Mouse Model for Salmonella Diarrhea

Tsuyoshi Miki, Ryosuke Goto, Mayuka Fujimoto, Nobuhiko Okada, Wolf-Dietrich Hardt

Cell Host Microbe. (2017) Feb 8;21(2):195-207

Speaker: Shih-Hsuan Lin (林詩璇)                               Time: 14:00~15:00, Apr. 25, 2018

Commentator: Dr. Pei-Jane Tsai (蔡佩珍老師)     Place: Room 601

Abstract:

Salmonella enterica serovars Typhimurium (S. Typhimurium) is a common enteropathogenic bacteria causing food-borne diarrhea. S. Typhimurium has been shown to invade intestinal epithelial cells and induce an inflammatory response. Inflammation prolongs the colonization of S. Typhimurium in the intestine of mice ⁽¹⁾. At the later stage of infection, the gut microbiota, a commensal microbial community, regrows and outcompetes S. Typhimurium ⁽²⁾. However, additional mechanisms that how pathogen eliminated from the gut lumen at the end of acute infections are still unclear. One of the antimicrobials, RegIIIβ, is a bactericidal lectin secreted by intestinal epithelial cells. They not only kill some pathogens, but also some commensal bacteria ⁽³⁾. Therefore, RegIIIβ effects microbiota composition and establishes intestinal homeostasis. In this study, the authors used wildtype and RegIIIβ^-/- mice to demonstrate that RegIIIβ could promote S. Typhimurium colonization and reduced the composition of Bacteriodes spp. in the inflamed gut. Further analyzing the key metabolite of the inflamed gut showed RegIIIβ expression suppressed luminal vitamin B6 levels. Moreover, supplementation with Bacteroides spp. or vitamin B6 accelerated clearance of pathogen from the gut. These findings indicated that RegIIIβ effected the level of Bacteriodes spp. and vitamin B6 in the gut lumen. Results from this study uncovered a new avenues therapeutic for Salmonella colitis that intervening at the level of RegIIIβ, and supplementing with Bacteroides spp. or vitamin B6.

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