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Salmonella-induced mucosal lectin RegIIIβ kills competing gut microbiota.

Stelter C, Käppeli R, König C, Krah A, Hardt WD, Stecher B, Bumann D - PLoS ONE (2011)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Junior Group, Mucosal Infections, Institute of Immunology, Hannover Medical School, Hannover, Germany.

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. 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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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.
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pone-0020749-g004: 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.

Mentions: All S. Typhimurium strains used in this study were derivatives of SL1344 hisG rpsL xyl [32] (TABLE 1). The virulent and avirulent S. Typhimurium strains have been described previously [33], [34] as well as S. Typhimurium ΔaroA [35]. Salmonella Typhimurium mutants with defined gene deletions were obtained using the Lambda phage red recombinase method [36] with primers described at http://falkow.stanford.edu/whatwedo/wanner/ (see also TABLE 2). For comparison of LPS defect mutants, Salmonella Typhimurium LT galE [37] was used.


Salmonella-induced mucosal lectin RegIIIβ kills competing gut microbiota.

Stelter C, Käppeli R, König C, Krah A, Hardt WD, Stecher B, Bumann D - PLoS ONE (2011)

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.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3111430&req=5

pone-0020749-g004: 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.
Mentions: All S. Typhimurium strains used in this study were derivatives of SL1344 hisG rpsL xyl [32] (TABLE 1). The virulent and avirulent S. Typhimurium strains have been described previously [33], [34] as well as S. Typhimurium ΔaroA [35]. Salmonella Typhimurium mutants with defined gene deletions were obtained using the Lambda phage red recombinase method [36] with primers described at http://falkow.stanford.edu/whatwedo/wanner/ (see also TABLE 2). For comparison of LPS defect mutants, Salmonella Typhimurium LT galE [37] was used.

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Junior Group, Mucosal Infections, Institute of Immunology, Hannover Medical School, Hannover, Germany.

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. 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.

Show MeSH
Related in: MedlinePlus