ArticleThe Journal of clinical investigation2014
CXCL5-secreting pulmonary epithelial cells drive destructive neutrophilic inflammation in tuberculosis.
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.
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Who cites it
139 citing papers in PubMed, 219 citations in OpenAlex.
- Early mucosal responses following a randomised controlled human inhaled infection with attenuated Mycobacterium bovis BCG.Nature communications · 2025Trial
- Pathogenesis of Tuberculosis: Interplay Between Host Antituberculosis Immunity and Immune Evasion Strategies ofMedComm · 2026Review
- Influenza-induced tuft cell expansion alters ILC-mediated inflammation.bioRxiv : the preprint server for biology · 2026Article
- VEGFR Blockade ReducesCells · 2026Article
- Single-cell and spatial profiling highlights TB-induced myofibroblasts as drivers of lung pathology.The Journal of experimental medicine · 2026Article
- Structural and Functional Characterization of Protein Adhesins and Pili in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Article
- Hepatocyte iron suppresses liver fibrosis via fibrolytic neutrophil recruitment in cholestasis.JHEP reports : innovation in hepatology · 2025Article
- Decoding the Gut Microbiome in Primary Sjögren's Syndrome and Primary Biliary Cholangitis: Shared Dysbiosis, Distinct Patterns, and Associations with Clinical Features.Microorganisms · 2025Article
- Eosinophil-derived interleukin-24 compromises epithelial integrity and aggravates airway remodeling in mouse models of allergic asthma.Nature communications · 2025Article
- Mycobacterium tuberculosis-specific T cells restrain anti-cancer drug-induced neutrophilic lung inflammation in tuberculosis.Nature communications · 2025Article
- Lung epithelial injury impairs early host immune responses to Mycobacterium tuberculosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- In vivo regulation of the monocyte phenotype by Mycobacterium marinum and the ESX-1 type VII secretion system.Scientific reports · 2025Article
- Pathogenic role for CD101-negative neutrophils in the type I interferon-mediated immunopathogenesis of tuberculosis.Cell reports · 2025Article
- The autoimmune disease risk variant NCF1-His90 is associated with a reduced risk of tuberculosis in women.Frontiers in immunology · 2025Article
- The importance of inflammatory biomarkers in detecting and managing latent tuberculosis infection.Frontiers in immunology · 2025Review
- Cellular and Molecular Network Characteristics ofInternational journal of molecular sciences · 2024Article
- Article
- Dual neutrophil subsets exacerbate or suppress inflammation in tuberculosis via IL-1β or PD-L1.Life science alliance · 2024Article
- Mycobacterium tuberculosis strain with deletions in menT3 and menT4 is attenuated and confers protection in mice and guinea pigs.Nature communications · 2024Article
- Bulk RNA sequencing of human pediatric lung cell populations reveals unique transcriptomic signature associated with postnatal pulmonary development.American journal of physiology. Lung cellular and molecular physiology · 2024Article
79 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Successful host defense against numerous pulmonary infections depends on bacterial clearance by polymorphonuclear leukocytes (PMNs); however, excessive PMN accumulation can result in life-threatening lung injury. Local expression of CXC chemokines is critical for PMN recruitment. The impact of chemokine-dependent PMN recruitment during pulmonary Mycobacterium tuberculosis infection is not fully understood. Here, we analyzed expression of genes encoding CXC chemokines in M. tuberculosis-infected murine lung tissue and found that M. tuberculosis infection promotes upregulation of Cxcr2 and its ligand Cxcl5. To determine the contribution of CXCL5 in pulmonary PMN recruitment, we generated Cxcl5(-/-) mice and analyzed their immune response against M. tuberculosis. Both Cxcr2(-/-) mice and Cxcl5(-/-) mice, which are deficient for only one of numerous CXCR2 ligands, exhibited enhanced survival compared with that of WT mice following high-dose M. tuberculosis infection. The resistance of Cxcl5(-/-) mice to M. tuberculosis infection was not due to heightened M. tuberculosis clearance but was the result of impaired PMN recruitment, which reduced pulmonary inflammation. Lung epithelial cells were the main source of CXCL5 upon M. tuberculosis infection, and secretion of CXCL5 was reduced by blocking TLR2 signaling. Together, our data indicate that TLR2-induced epithelial-derived CXCL5 is critical for PMN-driven destructive inflammation in pulmonary tuberculosis.
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