Surface-Associated Lipoproteins Link Virulence to Colitogenic Activity in IL-10-Deficient Mice Independent of Their Expression Levels
Enterococcus faecalis is a commensal of the human intestinal core microbiota harboring several putative virulence factors, which highlight its role as opportunistic pathogen. This dualistic character is supported by recent evidence linking Enterococcus spp. to the pathogenesis of inflammatory bowel diseases (IBD). Although several studies suggest a crucial role for opportunistic pathogens in IBD pathogenesis targeting genetically susceptible individuals, the dynamic relationship between disease-relevant host compartments and specific bacterial structures able to trigger intestinal inflammation remain unclear. Here, we report that cell surface-associated lipoproteins and the enterococcal polysaccharide antigen, which are relevant for E. faecalis virulence in invertebrate infection models, but whose expression is minimally affected by the intestinal inflammatory milieu, exhibit colitogenic activity in a mouse model susceptible for chronic colitis. Bacterial lipoproteins trigger innate immune cell activation and are a critical prerequisite for E. faecalis-induced colitis. The enterococcal polysaccharide antigen mediates bacterial mucus penetration and adhesion to mucosal surfaces, promotes the formation of biofilm and contributes to E. faecalis colitogenic activity. Using E. faecalis as a model organism, we demonstrate that colitogenic activity of opportunistic pathogens can be assigned to specific bacterial structures, a finding that may help to identify the most essential steps in IBD-related microbe-host interactions.
Vyšlo v časopise:
Surface-Associated Lipoproteins Link Virulence to Colitogenic Activity in IL-10-Deficient Mice Independent of Their Expression Levels. PLoS Pathog 11(6): e32767. doi:10.1371/journal.ppat.1004911
Kategorie:
Research Article
prolekare.web.journal.doi_sk:
https://doi.org/10.1371/journal.ppat.1004911
Souhrn
Enterococcus faecalis is a commensal of the human intestinal core microbiota harboring several putative virulence factors, which highlight its role as opportunistic pathogen. This dualistic character is supported by recent evidence linking Enterococcus spp. to the pathogenesis of inflammatory bowel diseases (IBD). Although several studies suggest a crucial role for opportunistic pathogens in IBD pathogenesis targeting genetically susceptible individuals, the dynamic relationship between disease-relevant host compartments and specific bacterial structures able to trigger intestinal inflammation remain unclear. Here, we report that cell surface-associated lipoproteins and the enterococcal polysaccharide antigen, which are relevant for E. faecalis virulence in invertebrate infection models, but whose expression is minimally affected by the intestinal inflammatory milieu, exhibit colitogenic activity in a mouse model susceptible for chronic colitis. Bacterial lipoproteins trigger innate immune cell activation and are a critical prerequisite for E. faecalis-induced colitis. The enterococcal polysaccharide antigen mediates bacterial mucus penetration and adhesion to mucosal surfaces, promotes the formation of biofilm and contributes to E. faecalis colitogenic activity. Using E. faecalis as a model organism, we demonstrate that colitogenic activity of opportunistic pathogens can be assigned to specific bacterial structures, a finding that may help to identify the most essential steps in IBD-related microbe-host interactions.
Zdroje
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