ArticleCommunications biology2024
Pneumococcal pneumonia is driven by increased bacterial turnover due to bacteriocin-mediated intra-strain competition.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- From predicted bacteriocins to ecological function.Current research in microbial sciences · 2026Review
- Nasopharyngeal microbiota profiles and lytA-PCR status in adult pneumococcal pneumonia: distinct microbial communities and diagnostic implications.Pneumonia (Nathan Qld.) · 2026Article
- An unrecognized host response to microbial exposure resets circadian timing.bioRxiv : the preprint server for biology · 2026Article
- Quantifying host-microbe interactions with bacterial lineage tracing.Science (New York, N.Y.) · 2026Review
- Transcriptomic analysis ofMicrobial genomics · 2025Article
- Article
- Vibrio cholerae motility is associated with inter-animal transmission.Nature communications · 2025Article
- Colonization dynamics ofInfection and immunity · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Using chromosomal barcoding, we observed that >97% of the Streptococcus pneumoniae (Spn) population turns over in the lung within 2 days post-inoculation in a murine model. This marked collapse of diversity and bacterial turnover was associated with acute inflammation (severe pneumococcal pneumonia), high bacterial numbers in the lungs, bacteremia, and mortality. Intra-strain competition mediated by the blp locus, which expresses bacteriocins in a quorum-sensing-dependent manner, was required for each of these effects. Bacterial turnover from the activity of Blp-bacteriocins increased the release of the pneumococcal toxin, pneumolysin (Ply), which was sufficient to account for the lung pathology. The ability of Ply to evade complement, rather than its pore-forming activity, prevented opsonophagocytic clearance of Spn enabling its multiplication in the lung, facilitating the inflammatory response and subsequent invasion into the bloodstream. Thus, our study demonstrates how an appreciation for bacterial population dynamics during infection provides new insight into pathogenesis.
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Registered trials
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