ArticlePLoS pathogens2024
Fatty acid metabolism in neutrophils promotes lung damage and bacterial replication during tuberculosis.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Article
- Post-Tuberculosis Lung Disease: Clinicopathologic Insights, Diagnosis, Prevention, and Management.MedComm · 2026Review
- Exploring the impact of nutrition and autophagy on infectious diseases to inform the development of homeostatic-nanomedicines for HIV-TB coinfections.Discover nano · 2026Review
- Lipid droplet profiling during neutrophil differentiation by stimulated Raman scattering microscopy.Biotechnology progress · 2026Article
- Neutrophils and tuberculosis - insights into immunobiology and pathogenesis.Molecular biology reports · 2026Review
- Organelle interplay in host responses and mycobacterial resilience.EMBO reports · 2026Review
- Lipid metabolism in homeostasis and disease.Signal transduction and targeted therapy · 2026Review
- Granuloma dual RNA-seq reveals composite transcriptional programs driven by neutrophils and necrosis within tuberculous granulomas.Science advances · 2026Article
- Immunotherapy for tuberculosis: emerging modalities, cross-disciplinary innovations, and roadmaps for drug-resistant disease.Frontiers in immunology · 2026Review
- Essential redundancies fuel Mycobacterium tuberculosis adaptation to the host.PLoS pathogens · 2025Review
- Iodothyronine deiodinases in patients with stable chronic obstructive pulmonary disease - preliminary results.Pharmacological reports : PR · 2025Observational
- Neutrophil TLR2 signaling promotes lipid accumulation and vascular plaque growth.bioRxiv : the preprint server for biology · 2025Article
- Metabolic Changes in Zebrafish Larvae Infected withMetabolites · 2025Article
- Diagnostic value of neutrophil-to-lymphocyte ratio, fibrinogen-to-albumin ratio and red blood cell distribution width in tuberculosis combined with other bacterial infections.BMC pulmonary medicine · 2025Article
- Fatty acid metabolism in gouty arthritis: mechanisms to therapeutic targeting.Frontiers in immunology · 2025Review
- Thyroid Hormone Pathways in Respiratory Diseases: Mechanism and Therapeutic Potential.Journal of inflammation research · 2025Article
- Microenvironments of tuberculous granuloma: advances and opportunities for therapy.Frontiers in immunology · 2025Review
- Targeting macrophage metabolic checkpoints: a host-directed strategy to overcome drug tolerance in tuberculosis.Therapeutic advances in infectious diseaseArticle
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Mycobacterium tuberculosis (Mtb) infection induces a marked influx of neutrophils into the lungs, which intensifies the severity of tuberculosis (TB). The metabolic state of neutrophils significantly influences their functional response during inflammation and interaction with bacterial pathogens. However, the effect of Mtb infection on neutrophil metabolism and its consequent role in TB pathogenesis remain unclear. In this study, we examined the contribution of glycolysis and fatty acid metabolism on neutrophil responses to Mtb HN878 infection using ex-vivo assays and murine infection models. We discover that blocking glycolysis aggravates TB pathology, whereas inhibiting fatty acid oxidation (FAO) yields protective outcomes, including reduced weight loss, immunopathology, and bacterial burden in lung. Intriguingly, FAO inhibition preferentially disrupts the recruitment of a pathogen-permissive immature neutrophil population (Ly6Glo/dim), known to accumulate during TB. Targeting carnitine palmitoyl transferase 1a (Cpt1a)-a crucial enzyme in mitochondrial β-oxidation-either through chemical or genetic methods impairs neutrophils' ability to migrate to infection sites while also enhancing their antimicrobial function. Our findings illuminate the critical influence of neutrophil immunometabolism in TB pathogenesis, suggesting that manipulating fatty acid metabolism presents a novel avenue for host-directed TB therapies by modulating neutrophil functions.
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