ArticleNature communications2025
Reprogramming aerobic metabolism mitigates Streptococcus pyogenes tissue damage in a mouse necrotizing skin infection model.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Article
- Lysosomal permeabilization by Group AInfection and immunity · 2026Article
- Mechanisms underlying pyogenic bacterial infections of the skin.Archives of microbiology · 2026Review
- Tunable TriPcides suppress virulence factor secretion duringScience advances · 2026Article
- Staphylococcus aureus adapts to the host nutritional environment by coordinating the activity of central metabolic enzymes.PLoS pathogens · 2026Article
- Carbon metabolism and niche adaptation inmSphere · 2026Review
- An acetylation-dependent switch underlies host disease tolerance during streptococcal infection.Scientific reports · 2026Article
- Article
- Lysosomal permeabilization by Group AbioRxiv : the preprint server for biology · 2025Article
- Pathological neutrophil extracellular traps hinder postoperative anal fistula wound healing and are attenuated by Zuoqing granule via suppression of the Nox4 pathway.Frontiers in immunology · 2025Article
- Review
- Immunometabolic reprogramming in diabetic osteomyelitis: from mechanisms to therapeutics.Frontiers in cellular and infection microbiology · 2025Review
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8 authors.
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Abstract
Disease tolerance is a host response to infection that limits collateral damage to host tissues while having a neutral effect on pathogen fitness. Previously, we found that the pathogenic lactic acid bacterium Streptococcus pyogenes manipulates disease tolerance using its aerobic mixed-acid fermentation pathway via the enzyme pyruvate dehydrogenase, but the microbe-derived molecules that mediate communication with the host's disease tolerance pathways remain elusive. Here we show in a murine model that aerobic mixed-acid fermentation inhibits the accumulation of inflammatory cells including neutrophils and macrophages, reduces the immunosuppressive cytokine interleukin-10, and delays bacterial clearance and wound healing. In infected macrophages, the aerobic mixed-acid fermentation end-products acetate and formate from streptococcal upregulate host acetyl-CoA metabolism and reduce interleukin-10 expression. Inhibiting aerobic mixed-acid fermentation using a bacterial-specific pyruvate dehydrogenase inhibitor reduces tissue damage during murine infection, correlating with increased interleukin-10 expression. Our results thus suggest that reprogramming carbon flow provides a therapeutic strategy to mitigate tissue damage during infection.
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