Salmonella-Induced Mucosal Lectin RegIIIβ Kills Competing Gut Microbiota

作者：Christian Stelter, Rina Käppeli, Claudia König, Alexander Krah, Wolf‐Dietrich Hardt, Bärbel Stecher, Dirk Bumann · 发表于：PLoS ONE · 年份：2011 · DOI：10.1371/journal.pone.0020749 · 被引用次数：127 · 研究领域：Escherichia coli research studies、Salmonella and Campylobacter epidemiology、Viral gastroenteritis research and epidemiology

Intestinal inflammation induces alterations of the gut microbiota and promotes overgrowth of the enteric pathogen Salmonella enterica by largely unknown mechanisms. Here, we identified a host factor involved in this process. Specifically, the C-type lectin RegIIIβ is strongly upregulated during mucosal infection and released into the gut lumen. In vitro, RegIIIβ kills diverse commensal gut bacteria but not Salmonella enterica subspecies I serovar Typhimurium (S. Typhimurium). Protection of the pathogen was attributable to its specific cell envelope structure. Co-infection experiments with an avirulent S. Typhimurium mutant and a RegIIIβ-sensitive commensal E. coli strain demonstrated that feeding of RegIIIβ was sufficient for suppressing commensals in the absence of all other changes inflicted by mucosal disease. These data suggest that RegIIIβ production by the host can promote S. Typhimurium infection by eliminating inhibitory gut microbiota.