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. 2011;6(6):e20749.
doi: 10.1371/journal.pone.0020749. Epub 2011 Jun 9.

Salmonella-induced mucosal lectin RegIIIβ kills competing gut microbiota

Christian Stelter  1 , Rina Käppeli, Claudia König, Alexander Krah, Wolf-Dietrich Hardt, Bärbel Stecher, Dirk Bumann
Affiliations

Salmonella-induced mucosal lectin RegIIIβ kills competing gut microbiota

Christian Stelter et al. PLoS One. 2011.

Abstract

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 VSports手机版. 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. .

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. S. Typhimurium-induced RegIIIβ expression in mouse intestine.
A) RegIIIβ expression was analyzed in the cecum of streptomycin-treated C57BL/6 mice infected for 24 h with S. Typhimurium wt and S. Typhimurium avir, respectively. Expression was analyzed by quantitative real time PCR normalized to GAPDH mRNA levels (fold expression versus unmanipulated mouse). B) Western Blot of intestinal contents obtained from S. Typhimurium infected MyD88+/− and MyD88−/− litter mates 24 h post infection using a polyclonal antibody to RegIIIβ. Samples 1–3 were obtained from infected MyD88+/− mice and samples 4–6 from MyD88−/− litter mates. C) Immunohistochemistry of the cecal mucosa of S. Typhimurium infected mice 24 h post infection (grey, nuclei (DAPI); blue, actin (phalloidin); red, RegIIIβ). Scale bar: 10 µm.
Figure 2
Figure 2. RegIIIβ has bactericidal activity against several Gram+ and Gram− intestinal bacteria.
A) Survival of S. Typhimurium (filled circles), E. coli (open circles), and Bacillus subtilis (triangles) after 30 min incubation with various concentrations of RegIIIβ. Means ± SD of five independent replicates are shown. B) Survival of various intestinal commensal bacteria after incubation with 10 µM RegIIIβ (1, E. coli Nissle; 2, E. coli CFT073; 3, Lactobacillus reuteri; 4, Lactobacillus murinus; 5, Enterococcus faecalis; 6, Clostridium butyricum). C) Bactericidal activities of 10 µM RegIIIβ and 10 µM RegIIIβ R135T with altered putative binding site against S. Typhimurium, E. coli and B. subtilis (symbols as in A). Statistical significances for deviation from results obtained for bacteria incubated with buffer only are shown.
Figure 3
Figure 3. The O-antigen mediates S. Typhimurium resistance against RegIIIβ.
A) SDS-PAGE (silver stain) of lipopolysaccharide of wild-type S. Typhimurium (lane 1) and mutants (phoP, rfc, rfbP, galE, rfaG). B) Bactericidal activity of 10 µM RegIIIβ against various S. Typhimurium mutants. Statistical significances for deviation from results obtained for wildtype bacteria are shown. C) Schematic representation of Salmonella spp. LPS-forms.
Figure 4
Figure 4. RegIIIβ is sufficient to suppress E. coli during competitive growth in the non-inflamed gut.
A) Colonization of streptomycin-pretreated mice with virulent S. Typhimurium wt (filled circles) and non-pathogenic E. coli E2 (open circles). Virulent S. Typhimurium induces gut inflammation and suppresses co-colonization with E. coli. B) Avirulent S. Typhimurium permits E. coli co-colonization. C) A single dose of RegIIIβ is sufficient to complement the suppression defect of avirulent S. Typhimurium. Each data point represents one mouse. Statistical significances for deviation from results obtained at 5 h are shown.
Figure 5
Figure 5. RegIIIβ facilitates S. Typhimurium colonization in mice with complex microbiota.
A) Colonization of mice with normal intestinal microbiota (no streptomycin pre-treatment) with facultative aerobes (open circles, colonies on MacConkey agar plates; left). Colonization levels of facultative aerobes after a single oral dose of BSA or RegIIIβ and subsequent infection with S. Typhimurium (closed circles; middle and right). A single dose of RegIIIβ suppressed resident facultative aerobic bacteria and partially relieved colonization resistance against S. Typhimurium. Statistical significances for deviation from results obtained with BSA alone are shown. B) RegIIIβ facilitates prolonged gut colonization by avirulent S. Typhimurium in streptomycin-pretreated mice. Daily RegIIIβ doses (80 µg in 200 µl) prolonged S. Typhimurium colonization (filled down triangles) compared to control mice that received bovine serum albumin (open up triangles). In panel A) one data point represents one mouse; in panel B) one data point represents the median with SD of 5 mice. Statistical significances for deviation from results obtained for BSA alone are shown. Comparable data were obtained in an independent experiment.
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