ArticleThe Journal of infectious diseases2013
Role of interleukin 6 in innate immunity to Mycobacterium tuberculosis infection.
Article in The Journal of infectious diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 162 citations in OpenAlex.
- Trial
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- B cells and iBALT in TB immunity & pathogenesis.Frontiers in immunology · 2026Review
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- GATA2 mutation is associated with immune dysfunction and increased Mycobacterium haemophilum susceptibility in immunocompromised individuals.JCI insight · 2025Article
- The Role of Salivary Diagnostic Techniques in Screening for Active Pulmonary Tuberculosis: A Systematic Review and Meta-Analysis.Microorganisms · 2025Review
- The Role of Inflammation in the Pathogenesis of Comorbidity of Chronic Obstructive Pulmonary Disease and Pulmonary Tuberculosis.International journal of molecular sciences · 2025Review
- Multiplexed cytokine profiling identifies diagnostic signatures for latent tuberculosis and reactivation risk stratification.PloS one · 2025Article
- Reduced fitness and enhanced immunogenicity ofCurrent research in microbial sciences · 2025Article
- Performance of eight serum cytokine/chemokine biomarkers in discriminating between active and latent tuberculosis infection in Ghana.Frontiers in immunology · 2025Article
- Metabolic and immune consequences of antibiotic related microbiome alterations during first-line tuberculosis treatment in Bamako, Mali.Frontiers in immunology · 2025Article
- Single nucleotide polymorphisms in IFN-gamma, TNF-alpha, IL-6, IL-10, and TGF-beta in pulmonary and extrapulmonary tuberculosis in the State of Ceará, northeastern Brazil.Memorias do Instituto Oswaldo Cruz · 2025Article
- Transcriptional profile ofiScience · 2024Article
- Regulation of ROS metabolism in macrophage via xanthine oxidase is associated with disease progression in pulmonary tuberculosis.Metabolomics : Official journal of the Metabolomic Society · 2024Article
- Analysis of alpha-1-antitrypsin (AAT)-regulated, glucocorticoid receptor-dependent genes in macrophages reveals a novel host defense function of AAT.Physiological reports · 2024Article
- The Influence of Body Fat Dynamics on Pulmonary Immune Responses in Murine Tuberculosis: Unraveling Sex-Specific Insights.International journal of molecular sciences · 2024Article
- Clinical features, immunologic parameter and treatment outcome of Chinese tuberculosis patients with or without DM.Frontiers in medicine · 2024Article
25 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundMycobacterium tuberculosis can grow in the hostile intracellular environment of macrophages by actively evading macrophage-associated antibacterial activities. The stress response factor SigH contributes to this process by modulating β-chemokine and interleukin 6 (Il6) expression. Hence, Il6 is of critical importance for acquired immunity against M. tuberculosis infection. Here, we attempted to better characterize the role of Il6 in the immune response to M. tuberculosis infection.
methodsA small interfering RNA-based approach was used to silence expression of the Il6 transcript in host macrophages infected with a wild-type strain of M. tuberculosis or an attenuated mutant strain of M. tuberculosis (Mtb:Δ-sigH). The outcome was measured by the analysis of bacterial burden and transcriptome-wide analysis of host gene expression. Transcriptome results were confirmed via quantitative polymerase chain reaction and enzyme-linked immunosorbent assay.
resultsWild type and Mtb:Δ-sigH infection of host macrophages in which Il6 had been silenced resulted in increased expression of interferon-inducible genes, especially those involved in type I interferon signaling. The expression of Ly-6 genes was significantly higher in cells infected with Mtb:Δ-sigH, compared with those infected with the wild-type strain (P < .05).
conclusionsM. tuberculosis regulates host Il6 production to inhibit type I interferon signaling and, consequently, disease progression. Mtb:Δ-sigH is associated with delayed activation of macrophages, compared with the wild-type strain, and with delayed inflammatory stimuli as consequence. These findings have important implications for improving understanding of the mechanisms behind M. tuberculosis virulence and pathogenesis and provide an initial road map to further investigate the mechanisms that may account for the deleterious effects of type I interferons in M. tuberculosis infection.
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