ArticleNature communications2023
Quantitative dose-response analysis untangles host bottlenecks to enteric infection.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Prophage-encoding engineered bacteria enable prophylactic lytic phage therapy for enteric infection in mice.Nature microbiology · 2026Article
- Bi-directional highways and super-seeder tissues underpin parasite dissemination in experimental Leishmania donovani infection.Nature communications · 2026Article
- Metabolic strategies of Enterobacteriaceae gut colonization.Nature reviews. Microbiology · 2026Review
- Transcriptomic timeseries links hepatic gene expression to an early and self-limited systemic response to enteric infection.PLoS pathogens · 2026Article
- The cholesterol-dependent cytolysin promotesInfection and immunity · 2026Article
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- Vibrio cholerae serotype impacts pathogenicity.Nature communications · 2026Article
- Quantifying host-microbe interactions with bacterial lineage tracing.Science (New York, N.Y.) · 2026Review
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- Anoxia activates CRISPR-Cas immunity in the mouse intestine.Nature microbiology · 2025Article
- Article
- Applying ecological principles to microbiome engineering.Nature microbiology · 2025Review
- Vibrio cholerae motility is associated with inter-animal transmission.Nature communications · 2025Article
- Quantifying the intra- and inter-species community interactions in microbiomes by dynamic covariance mapping.Nature communications · 2025Article
- Article
- Inducible transposon mutagenesis identifies bacterial fitness determinants during infection in mice.Nature microbiology · 2025Article
- Monosaccharides drive Salmonella gut colonization in a context-dependent or -independent manner.Nature communications · 2025Article
- Quantification ofeLife · 2025Article
- The Mla pathway promotesmBio · 2025Article
- Patterns of Klebsiella pneumoniae bacteremic dissemination from the lung.Nature communications · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Host bottlenecks prevent many infections before the onset of disease by eliminating invading pathogens. By monitoring the diversity of a barcoded population of the diarrhea causing bacterium Citrobacter rodentium during colonization of its natural host, mice, we determine the number of cells that found the infection by establishing a replicative niche. In female mice the size of the pathogen's founding population scales with dose and is controlled by a severe yet slow-acting bottleneck. Reducing stomach acid or changing host genotype modestly relaxes the bottleneck without breaking the fractional relationship between dose and founders. In contrast, disrupting the microbiota causes the founding population to no longer scale with the size of the inoculum and allows the pathogen to infect at almost any dose, indicating that the microbiota creates the dominant bottleneck. Further, in the absence of competition with the microbiota, the diversity of the pathogen population slowly contracts as the population is overtaken by bacteria having lost the critical virulence island, the locus of enterocyte effacement (LEE). Collectively, our findings reveal that the mechanisms of protection by colonization bottlenecks are reflected in and can be generally defined by the impact of dose on the pathogen's founding population.
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