ArticleGenes & genomics2024
Mycobacterium tuberculosis virulence protein ESAT-6 influences M1/M2 polarization and macrophage apoptosis to regulate tuberculosis progression.
Article in Genes & genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- (Cu-S)Mikrochimica acta · 2026Article
- Lasting bone marrow defects imprinted by hyperglycemia shape the immunological characteristics of differentiated M1 and M2 macrophages.Genes & genomics · 2026Article
- Macrophage states and polarization duringFrontiers in cellular and infection microbiology · 2026Review
- A machine learning model and molecular clusters of epigenetic chromatin regulators in tuberculosis based on bioinformatics and clinical samples.Scientific reports · 2025Article
- Baicalein inhibits mycobacterium tuberculosis-induced macrophage M1 polarization depending on the regulation of YY1/RAB10/TLR4 pathway.Journal of inflammation (London, England) · 2025Article
- Immunoregulation by ESAT-6: From Pathogenesis of Tuberculosis to Potential Anti-Inflammatory and Anti-Rejection Application.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The exacerbating effects of stable pulmonary tuberculosis on the deterioration of inflammatory response, coagulation function, and pulmonary function in COPD: A propensity score-matched retrospective study.Journal of clinical tuberculosis and other mycobacterial diseases · 2025Article
- Tuberculosis Patients' Serum Extracellular Vesicles Induce Relevant Immune Responses for Initial Defense Against BCG in Mice.Microorganisms · 2025Article
- Multi-Omics Analysis of the Immune Effect of the Engineered Exosome Drug Delivery System in Inducing Macrophage Apoptosis.Pharmaceutics · 2025Article
- Article
- Ag85B-induced M1 Macrophage Polarization via the TLR4/TRAF6/NF-κB Axis Leading to Bronchial Epithelial Cell Damage and TH17/Treg Imbalance.Current molecular medicine · 2025Article
- Participants inFrontiers in immunology · 2025Review
- Depletion ofFrontiers in cellular and infection microbiology · 2025Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTuberculosis (TB) is an infectious disease caused by infection with Mycobacterium tuberculosis (Mtb), and it remains one of the major threats to human health worldwide. To our knowledge, the polarization of M1/M2 macrophages were critical innate immune cells which play important roles in regulating the immune response during TB progression.
objectiveWe aimed to explore the potential mechanisms of M1/M2 macrophage polarization in TB development.
methodsTHP-1 macrophages were treated with early secreted antigenic target of 6 kDa (ESAT-6) protein for an increasing time. The polarization profiles, apoptosis levels of M1 and M2 macrophages were detected by RT-qPCR, immunofluorescence, Western blot and flow cytometry.
resultsESAT-6 initially promoted the generation of pro-inflammatory M1-polarized macrophages in THP-1 cells within 24 h, which were suppressed by further ESAT-6 treatment at 30-42 h. Interestingly, ESAT-6 continuously promoted M2 polarization of THP-1 cells, thereby maintaining the anti-inflammatory response in a time-dependent manner. In addition, ESAT-6 promoted apoptotic cell death in M1-polarized macrophages, which had little effects on apoptosis of M2-phenotype of macrophages. Then, the potential underlying mechanisms were uncovered, and we verified that ESAT-6 increased the protein levels of TLR4, MyD88 and NF-κB to activate the TLR4/MyD88/NF-κB pathway within 24 h, and this signal pathway was significantly inactivated at 36 h post-treatment. Interestingly, the following experiments confirmed that ESAT-6 TLR4/MyD88/NF-κB pathway-dependently regulated M1/M2 polarization and apoptosis of macrophage in THP-1 cells.
conclusionOur study investigated the detailed effects and mechanisms of M1/M2 macrophages in regulating innate responses during TB development, which provided a new perspective on the development of treatment strategies for this disease.
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