ArticleThe Journal of biological chemistry2013
Endocytosis of Mycobacterium tuberculosis heat shock protein 60 is required to induce interleukin-10 production in macrophages.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
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- The SH3-binding domain of chorismate mutase protein ofiScience · 2024Article
- Diabetes and tuberculosis: An emerging dual threat to healthcare.World journal of diabetes · 2024Article
- From immunology to artificial intelligence: revolutionizing latent tuberculosis infection diagnosis with machine learning.Military Medical Research · 2023Review
- Role of pattern recognition receptors in sensingHeliyon · 2023Review
- The cause-effect relation of tuberculosis on incidence of diabetes mellitus.Frontiers in cellular and infection microbiology · 2023Review
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- Macrophage: A Cell With Many Faces and Functions in Tuberculosis.Frontiers in immunology · 2022Review
- Keratinocyte and Fibroblast Wound Healing In Vitro Is Repressed by Non-Optimal Conditions but the Reparative Potential Can Be Improved by Water-Filtered Infrared A.Biomedicines · 2021Article
- Nontuberculous Mycobacteria, Macrophages, and Host Innate Immune Response.Infection and immunity · 2021Review
- Interaction of TLR4 and TLR8 in the Innate Immune Response against Mycobacterium Tuberculosis.International journal of molecular sciences · 2021Article
- Single Nucleotide Polymorphisms in the Bovine TLR2 Extracellular Domain Contribute to Breed and Species-Specific Innate Immune Functionality.Frontiers in immunology · 2021Article
- Article
- Hacking the host: exploitation of macrophage polarization by intracellular bacterial pathogens.Pathogens and disease · 2020Review
- Target the Host, Kill the Bug; Targeting Host Respiratory Immunosuppressive Responses as a Novel Strategy to Improve Bacterial Clearance During Lung Infection.Frontiers in immunology · 2020Review
- Competitive Cell Death Interactions in Pulmonary Infection: Host Modulation Versus Pathogen Manipulation.Frontiers in immunology · 2020Review
- Fatty acylCoA synthetase FadD13 regulates proinflammatory cytokine secretion dependent on the NF-κB signalling pathway by binding to eEF1A1.Cellular microbiology · 2019Article
- Mycobacterium tuberculosis Exploits a Molecular Off Switch of the Immune System for Intracellular Survival.Scientific reports · 2018Article
- Molecular basis of mycobacterial survival in macrophages.Cellular and molecular life sciences : CMLS · 2017Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding the signaling pathways involved in the regulation of anti-inflammatory and pro-inflammatory responses in tuberculosis is extremely important in tailoring a macrophage innate response to promote anti-tuberculosis immunity in the host. Although the role of toll-like receptors (TLRs) in the regulation of anti-inflammatory and pro-inflammatory responses is known, the detailed molecular mechanisms by which the Mycobacterium tuberculosis bacteria modulate these innate responses are not clearly understood. In this study, we demonstrate that M. tuberculosis heat shock protein 60 (Mtbhsp60, Cpn60.1, and Rv3417c) interacts with both TLR2 and TLR4 receptors, but its interaction with TLR2 leads to clathrin-dependent endocytosis resulting in an increased production of interleukin (IL)-10 and activated p38 MAPK. Blockage of TLR2-mediated endocytosis inhibited IL-10 production but induced production of tumor necrosis factor (TNF)-α and activated ERK1/2. In contrast, upon interaction with TLR4, Mtbhsp60 remained predominantly localized on the cell surface due to poorer endocytosis of the protein that led to decreased IL-10 production and p38 MAPK activation. The Escherichia coli homologue of hsp60 was found to be retained mainly on the macrophage surface upon interaction with either TLR2 or TLR4 that triggered predominantly a pro-inflammatory-type immune response. Our data suggest that cellular localization of Mtbhsp60 upon interaction with TLRs dictates the type of polarization in the innate immune responses in macrophages. This information is likely to help us in tailoring the host protective immune responses against M. tuberculosis.
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