ArticleNature communications2025
A host-pathogen metabolic synchrony that facilitates disease tolerance.
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 13 papers.
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Who cites it
13 citing papers in PubMed.
- Itaconate: a dual-edged sword in immunometabolism and host-pathogen interactions.Archives of microbiology · 2026Review
- Host-pathogen pyrimidine metabolism drives cystic fibrosis lung disease.Nature communications · 2026Article
- Itaconate and its derivatives in human health and diseases.Signal transduction and targeted therapy · 2026Review
- Immune protection and persistence in Pseudomonas aeruginosa infections by pyruvate cross-feeding.Nature communications · 2026Article
- Offense and defense: itaconate mediates bidirectional immune regulation of host-bacteria interaction.Journal of biomedical science · 2026Review
- Heavy Metal-Driven Oral Dysbiosis: Salivary Toxicometallomics at the Host-Microbiome Interface Across Pathologies.Life (Basel, Switzerland) · 2026Review
- Itaconate modifications: Mechanisms and applications.Journal of intensive medicine · 2026Review
- Mutations in the mucA gene of Pseudomonas aeruginosa promote disease exacerbation.Archives of microbiology · 2026Review
- Immune evasion, dysregulation, and emerging immunotherapies for invasive fungal infections in the immunocompromised host.Frontiers in immunology · 2026Review
- How do immunometabolites shape bacterial infections?PLoS biology · 2026Article
- Airway immunometabolic responses during pulmonary bacterial and viral infections.Cell reports · 2025Review
- Sequestration of the phagocyte metabolite itaconate by Pseudomonas aeruginosa RpoN promotes successful pulmonary infection.Nature communications · 2025Article
- Fecal microbiota transplantation in pigs: current status and future perspective.Animal microbiome · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Disease tolerance mitigates organ damage from non-resolving inflammation during persistent infections, yet its underlying mechanisms remain unclear. Here we show, in a Pseudomonas aeruginosa pneumonia mouse model, that disease tolerance depends on the mitochondrial metabolite itaconate, which mediates cooperative host-pathogen interactions. In P. aeruginosa, itaconate modifies key cysteine residues in TCA cycle enzymes critical for succinate metabolism, inducing bioenergetic stress and promoting the formation biofilms that are less immunostimulatory and allow the bacteria to integrate into the local microbiome. Itaconate incorporates into the central metabolism of the biofilm, driving exopolysaccharide production-particularly alginate-which amplifies airway itaconate signaling. This itaconate-alginate interplay limits host immunopathology by enabling pulmonary glutamine assimilation, activating glutaminolysis, and thereby restrain detrimental inflammation caused by the inflammasome. Clinical sample analysis reveals that P. aeruginosa adapts to this metabolic environment through compensatory mutations in the anti-sigma-factor mucA, which restore the succinate-driven bioenergetics and disrupt the metabolic synchrony essential for sustaining disease tolerance.
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