ArticleScientific reports2017
Early Secreted Antigenic Target of 6-kDa of Mycobacterium tuberculosis Stimulates IL-6 Production by Macrophages through Activation of STAT3.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 60 citations in OpenAlex.
- Immunoregulation by ESAT-6: From Pathogenesis of Tuberculosis to Potential Anti-Inflammatory and Anti-Rejection Application.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Meprin β activity modulates cellular proliferation via trans-signaling IL-6-mediated AKT/ERK pathway in IR-induced kidney injury.BMC nephrology · 2025Article
- Immunogenicity and protective efficacy of a multi-antigenic adenovirus-based vaccine candidate againstFrontiers in microbiology · 2025Article
- Heterogeneity and interplay: the multifaceted role of cancer-associated fibroblasts in the tumor and therapeutic strategies.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Review
- Host Cell Death and Modulation of Immune Response againstInternational journal of molecular sciences · 2024Review
- Gut microbiome, T cell subsets, and cytokine analysis identify differential biomarkers in tuberculosis.Frontiers in immunology · 2024Article
- Impact ofFrontiers in immunology · 2024Article
- BCG revaccination in adults enhances pro-inflammatory markers of trained immunity along with anti-inflammatory pathways.iScience · 2023Article
- Turning foes into permissive hosts: manipulation of macrophage polarization by intracellular bacteria.Current opinion in immunology · 2023Review
- Advances of Long Non-Coding RNAs as Potential Biomarkers for Tuberculosis: New Hope for Diagnosis?Pharmaceutics · 2023Review
- Tumor cell plasticity in targeted therapy-induced resistance: mechanisms and new strategies.Signal transduction and targeted therapy · 2023Review
- Histone deacetylase-2 controls IL-1β production through the regulation of NLRP3 expression and activation in tuberculosis infection.iScience · 2022Article
- Early IL-17A production helps establish Mycobacterium intracellulare infection in mice.PLoS pathogens · 2022Article
- Ibrutinib reverses IL-6-induced osimertinib resistance through inhibition of Laminin α5/FAK signaling.Communications biology · 2022Article
- Sphingosine-1-phosphate receptors 2 and 3 reprogram resting human macrophages into M1 phenotype following mycobacteria infection.Current research in immunology · 2022Article
- Characterization of chemokine and cytokine expression pattern in tuberculous lymphadenitis patient.Frontiers in immunology · 2022Observational
- Potential ofOncoimmunology · 2022Article
- The role played by bacterial infections in the onset and metastasis of cancer.Current research in microbial sciences · 2021Review
- Exaggerated IL-17A activity in human in vivo recall responses discriminates active tuberculosis from latent infection and cured disease.Science translational medicine · 2021Article
- Subunit Vaccine ESAT-6:c-di-AMP Delivered by Intranasal Route Elicits Immune Responses and Protects AgainstFrontiers in cellular and infection microbiology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As early secreted antigenic target of 6 kDa (ESAT-6) of Mycobacterium tuberculosis (Mtb) is an essential virulence factor and macrophages are critical for tuberculosis infection and immunity, we studied ESAT-6 stimulated IL-6 production by macrophages. ESAT-6 stimulated significantly higher IL-6 secretion by murine bone marrow derived macrophages (BMDM) compared to culture filtrate protein 10 kDa (CFP10) and antigen 85A. Polymyxin B, an LPS blocker, did not affect ESAT-6 stimulated macrophage IL-6 production. ESAT-6 but not Pam3CSK4 induced IL-6 by TLR2 knockout BMDM. ESAT-6 induced phosphorylation and DNA binding of STAT3 and this was blocked by STAT3 inhibitors but not by rapamycin. STAT3 inhibitors suppressed ESAT-6-induced IL-6 transcription and secretion without affecting cell viability. This was confirmed by silencing STAT3 in macrophages. Blocking neither IL-6Rα/IL-6 nor IL-10 affected ESAT-6-induced STAT3 activation and IL-6 production. Infection of BMDM and human macrophages with Mtb with esat-6 deletion induced diminished STAT3 activation and reduced IL-6 production compared to wild type and esat-6 complemented Mtb strains. Administration of ESAT-6 but not CFP10 induced STAT3 phosphorylation and IL-6 expression in the mouse lungs, consistent with expression of ESAT-6, IL-6 and phosphorylated-STAT3 in Mtb-infected mouse lungs. We conclude that ESAT-6 stimulates macrophage IL-6 production through STAT3 activation.
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