ArticleCell death & disease2018
Clinical isolates of the modern Mycobacterium tuberculosis lineage 4 evade host defense in human macrophages through eluding IL-1β-induced autophagy.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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42 citing papers in PubMed, 61 citations in OpenAlex.
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- Comparative genomics and epidemic success of Mycobacterium tuberculosis lineage 4 in eastern China.BMC genomics · 2026Article
- The lipid language of tuberculosis:mBio · 2026Review
- From gum inflammation to oral cancers: pyroptosis as the molecular torchbearer in periodontitis-driven carcinogenesis.Discover oncology · 2025Review
- Immunologic cell deaths: involvement in the pathogenesis and intervention therapy of periodontitis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Soluble immune mediators orchestrate protectiveeLife · 2025Article
- Decoding the tuberculosis puzzle: mechanical factors driving disease progression.Frontiers in tuberculosis · 2025Article
- Management of tuberculosis risk, screening and preventive therapy in patients with chronic autoimmune arthritis undergoing biotechnological and targeted immunosuppressive agents.Frontiers in immunology · 2025Review
- Experimental dissection of tuberculosis protective immunity: a human perspective.Frontiers in cellular and infection microbiology · 2025Review
- Differential Host Gene Expression in Response to Infection by DifferentMicroorganisms · 2024Article
- Regulation of autophagy by protein lipidation.Advanced biotechnology · 2024Review
- An Update on the Study of the Molecular Mechanisms Involved in Autophagy during Bacterial Pathogenesis.Biomedicines · 2024Review
- Transcriptome analysis and molecular characterization of novel small RNAs in Mycobacterium tuberculosis Lineage 1.World journal of microbiology & biotechnology · 2024Article
- Bacterial diversity dominates variable macrophage responses of tuberculosis patients in Tanzania.Scientific reports · 2024Article
- Immunomodulatory effects of cysteamine and its potential use as a host-directed therapy for tuberculosis.Frontiers in immunology · 2024Article
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- Tuberculosis Severity Predictive Model Using Mtb Variants and Serum Biomarkers in a Colombian Cohort of APTB Patients.Biomedicines · 2023Article
- MDA5 RNA-sensing pathway activation by Mycobacterium tuberculosis promotes innate immune subversion and pathogen survival.JCI insight · 2023Article
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB), has infected over 1.7 billion people worldwide and causes 1.4 million deaths annually. Recently, genome sequence analysis has allowed the reconstruction of Mycobacterium tuberculosis complex (MTBC) evolution, with the identification of seven phylogeographic lineages: four referred to as evolutionarily "ancient", and three "modern". The MTBC strains belonging to "modern" lineages appear to show enhanced virulence that may have warranted improved transmission in humans over ancient lineages through molecular mechanisms that remain to be fully characterized. To evaluate the impact of MTBC genetic diversity on the innate immune response, we analyzed intracellular bacterial replication, inflammatory cytokine levels, and autophagy response in human primary macrophages infected with MTBC clinical isolates belonging to the ancient lineages 1 and 5, and the modern lineage 4. We show that, when compared to ancient lineage 1 and 5, MTBC strains belonging to modern lineage 4 show a higher rate of replication, associated to a significant production of proinflammatory cytokines (IL-1β, IL-6, and TNF-α) and induction of a functional autophagy process. Interestingly, we found that the increased autophagic flux observed in macrophages infected with modern MTBC is due to an autocrine activity of the proinflammatory cytokine IL-1β, since autophagosome maturation is blocked by an interleukin-1 receptor antagonist. Unexpectedly, IL-1β-induced autophagy is not disadvantageous for the survival of modern Mtb strains, which reside within Rab5-positive phagosomal vesicles and avoid autophagosome engulfment. Altogether, these results suggest that autophagy triggered by inflammatory cytokines is compatible with a high rate of intracellular bacilli replication and may therefore contribute to the increased pathogenicity of the modern MTBC lineages.
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