ArticleFrontiers in cellular and infection microbiology2015
Mycobacterium tuberculosis Infection Induces HDAC1-Mediated Suppression of IL-12B Gene Expression in Macrophages.
Article in Frontiers in cellular and infection microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Pooled it
- DNA methylation is associated with inhaled corticosteroid response in persistent childhood asthmatics.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2019Trial
- SH3PXD2B is the critical host factor promoting the entry of mycobacteria.Applied and environmental microbiology · 2026Article
- Epigenetic Reprogramming byAntibiotics (Basel, Switzerland) · 2026Review
- The Regulatory Effect of Histone Deacetylase (HDAC) 1 and 2 on iNOS, IL-6, TNF-α and IL-10 Expression in Canine Macrophages Infected With Leishmania infantum.Parasite immunology · 2026Article
- Construction of a DNA Methylation Map of Argali Hybrid Sheep During Mo Infection.Microorganisms · 2026Article
- Prolactin and 17β-Estradiol Are Epigenetic Regulators That Modify the Effector Response of Bovine Macrophages DuringMicroorganisms · 2026Article
- Reprogramming host histone modifications by bacterial pathogens.Molecules and cells · 2026Review
- HIV associated epigenetic trends and chronic diseases: insights into the hidden burden of chronic infection.Clinical epigenetics · 2026Review
- Macrophage states and polarization duringFrontiers in cellular and infection microbiology · 2026Review
- Cytotoxic granules and effector molecules from immune cells in tuberculosis: Mechanisms of host defense and therapeutic potential.Virulence · 2025Review
- The pathway of autophagy in the epigenetic landscape ofAutophagy · 2025Review
- The Role of Inflammation in the Pathogenesis of Comorbidity of Chronic Obstructive Pulmonary Disease and Pulmonary Tuberculosis.International journal of molecular sciences · 2025Review
- Pathogen-induced hijacking of host SUMOylation: from molecular mechanisms and prospects for therapeutic modulation.Frontiers in immunology · 2025Review
- Insights into the protein ubiquitinome in the host‒pathogen interplay duringFrontiers in molecular biosciences · 2025Article
- Sirtuin inhibitors reduce intracellular growth of M. tuberculosis in human macrophages via modulation of host cell immunity.Scientific reports · 2024Article
- Cleft lip and palate and periconception COVID-19 infection in five arab countries.Clinical oral investigations · 2024Article
- Article
- The Mycobacterium tuberculosis methyltransferase Rv2067c manipulates host epigenetic programming to promote its own survival.Nature communications · 2023Article
- Article
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
Downregulation of host gene expression is one of the many strategies employed by intracellular pathogens such as Mycobacterium tuberculosis (MTB) to survive inside the macrophages and cause disease. The underlying molecular mechanism behind the downregulation of host defense gene expression is largely unknown. In this study we explored the role of histone deacetylation in macrophages in response to infection by virulent MTB H37Rv in manipulating host gene expression. We show a significant increase in the levels of HDAC1 with a concomitant and marked reduction in the levels of histone H3-acetylation in macrophages containing live, but not killed, virulent MTB. Additionally, we show that HDAC1 is recruited to the promoter of IL-12B in macrophages infected with live, virulent MTB, and the subsequent hypoacetylation of histone H3 suppresses the expression of this gene which plays a key role in initiating Th1 responses. By inhibiting immunologically relevant kinases, and by knockdown of crucial transcriptional regulators, we demonstrate that protein kinase-A (PKA), CREB, and c-Jun play an important role in regulating HDAC1 level in live MTB-infected macrophages. By chromatin immunoprecipitation (ChIP) analysis, we prove that HDAC1 expression is positively regulated by the recruitment of c-Jun to its promoter. Knockdown of HDAC1 in macrophages significantly reduced the survival of intracellular MTB. These observations indicate a novel HDAC1-mediated epigenetic modification induced by live, virulent MTB to subvert the immune system to survive and replicate in the host.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.