ArticleMolecular and cellular biochemistry2019
Early secreted antigenic target of 6-kDa of Mycobacterium tuberculosis promotes caspase-9/caspase-3-mediated apoptosis in macrophages.
Article in Molecular and cellular biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Research progress in PANoptosis mechanisms and their interplay with tuberculosis.Frontiers in cellular and infection microbiology · 2026Review
- Article
- Functional analysis of type VII secretion system links to host immune evasion mechanism inFrontiers in cellular and infection microbiology · 2026Review
- Molecular links between tuberculosis and lung cancer: pathogenesis and therapeutic challenges.Archives of microbiology · 2025Review
- Immunoregulation by ESAT-6: From Pathogenesis of Tuberculosis to Potential Anti-Inflammatory and Anti-Rejection Application.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Early secretory antigen target of 6-kDa of Mycobacterium tuberculosis inhibits macrophage apoptosis and host defense via TLR2.Respiratory research · 2025Article
- Real-time visualization reveals Mycobacterium tuberculosis ESAT-6 disrupts phagosome-like compartment via fibril-mediated vesiculation.Cell reports · 2025Article
- ESAT-6 Modulates Macrophage Apoptosis in Mycobacterium Tuberculosis via lncNEAT1/miR-125b-5p/TNF-α Pathway.Infection and drug resistance · 2025Article
- The role of ESAT-6 in tuberculosis immunopathology.Frontiers in immunology · 2024Review
- Pathogen-driven nucleotide overload triggers mitochondria-centered cell death in phagocytes.PLoS pathogens · 2023Article
- An N-acetyltransferase required for EsxA N-terminal protein acetylation and virulence in Mycobacterium marinum.bioRxiv : the preprint server for biology · 2023Article
- Early activation of Toll-like receptor-3 reduces the pathological progression of Alzheimer's disease in APP/PS1 mouse.Alzheimer's research & therapy · 2023Article
- The Role of TLR2 in Infectious Diseases Caused by Mycobacteria: From Cell Biology to Therapeutic Target.Biology · 2022Review
- Macrophage: A Cell With Many Faces and Functions in Tuberculosis.Frontiers in immunology · 2022Review
- A Small Protein but with Diverse Roles: A Review of EsxA in Mycobacterium-Host Interaction.Cells · 2021Review
- The Common miRNAs between Tuberculosis and Non-Small Cell Lung Cancer: A Critical Review.Tanaffos · 2021Review
- Host-Pathogen Dialogues in Autophagy, Apoptosis, and Necrosis during Mycobacterial Infection.Immune network · 2020Review
- N-acetylcysteine (NAC) Attenuating Apoptosis and Autophagy in RAW264.7 Cells in Response to Incubation with Mycolic Acid from BovinePolish journal of microbiology · 2020Article
- Exploring the Molecular Intersection of Posterior Ocular Tuberculosis:Ophthalmology scienceArticle
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Mycobacterium tuberculosis (Mtb) is an intracellular pathogen that triggers several survival mechanisms against the host immune system. Many studies show that the diverse components of Mtb can modulate apoptosis in various types of cells differently. So far, apoptosis induced by ESAT-6, an early secreted antigenic target of 6-kDa of Mtb, has been studied but the details of molecular mechanism and signaling pathway remain incompletely defined. This study investigated the role of recombinant ESAT-6 in inducing apoptosis in primary bone marrow-derived macrophages (BMDMs) of mice using Annexin V/PI assay with FACS analysis and Western blotting technique. It has been found that ESAT-6-induced apoptosis in BMDMs in a dose- and time-dependent pattern. Apoptosis induced by ESAT-6 was mainly via the intrinsic pathway with elevated protein levels of cleaved caspase-9 and -3. Furthermore, ESAT-6 also induced Bim activation during this process. Interestingly, this event was TLR2-dependent since the effect of ESAT-6 on apoptosis vanished in BMDM from mice with TLR2 deficiency. Furthermore, ROS generation and MAPKs phosphorylation induced by ESAT-6 were also involved in caspase-9 and caspase-3 activation. Taken together, these data suggest that ESAT-6-mediated apoptosis is involved in ROS-MAPKs signaling and further activating the intrinsic pathway, which provides new insights into the basic physiology of macrophage death in tuberculosis.
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Registered trials
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