ArticlePLoS biology2007
Salmonella enterica serovar typhimurium exploits inflammation to compete with the intestinal microbiota.
Article in PLoS biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 615 papers.
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Who cites it
615 citing papers in PubMed.
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- Salmonella-derived haem inhibits macrophage phagocytosis and promotes infection in mice.Nature microbiology · 2026Article
- Antibiotic-induced gut microbiome dysbiosis: risks and strategies for mitigation.The EMBO journal · 2026Review
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- Exacerbated salmonellosis in poly(ADP-ribose) polymerase 14-deficient mice.Microbiology spectrum · 2026Article
- Changes in the gill and gut microbiota of koi infected with carp edema virus.Veterinary research · 2026Article
- Decoding the spatiotemporal heterogeneity of bacterial virulence gene expression using single-cell approaches.Frontiers in microbiology · 2026Review
- Gut microbiota dysbiosis: Pathogenic drivers and emerging phage-based therapeutics.AIMS microbiology · 2026Review
- Infection strategies ofGut microbes reports · 2026Review
555 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Most mucosal surfaces of the mammalian body are colonized by microbial communities ("microbiota"). A high density of commensal microbiota inhabits the intestine and shields from infection ("colonization resistance"). The virulence strategies allowing enteropathogenic bacteria to successfully compete with the microbiota and overcome colonization resistance are poorly understood. Here, we investigated manipulation of the intestinal microbiota by the enteropathogenic bacterium Salmonella enterica subspecies 1 serovar Typhimurium (S. Tm) in a mouse colitis model: we found that inflammatory host responses induced by S. Tm changed microbiota composition and suppressed its growth. In contrast to wild-type S. Tm, an avirulent invGsseD mutant failing to trigger colitis was outcompeted by the microbiota. This competitive defect was reverted if inflammation was provided concomitantly by mixed infection with wild-type S. Tm or in mice (IL10(-/-), VILLIN-HA(CL4-CD8)) with inflammatory bowel disease. Thus, inflammation is necessary and sufficient for overcoming colonization resistance. This reveals a new concept in infectious disease: in contrast to current thinking, inflammation is not always detrimental for the pathogen. Triggering the host's immune defence can shift the balance between the protective microbiota and the pathogen in favour of the pathogen.
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Registered trials
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