ArticleJournal of cellular and molecular medicine2019
HMGN2 regulates non-tuberculous mycobacteria survival via modulation of M1 macrophage polarization.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- High-mobility group N proteins are required for regulation of antigen-presentation genes in macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Nontuberculous Mycobacteria Infections in Children: A Clinical Overview of Diagnosis and Management.Microorganisms · 2026Review
- Exploring the effect and mechanism of baicalin on sepsis-induced acute lung injury based on network pharmacology and experimental verification.Scientific reports · 2025Article
- Deficiency of HMGN2 enhances antibacterial activity of macrophages by promoting H3 histone modification-mediated CD14/iNOS expression.Frontiers in immunology · 2025Article
- Epigenetic Mechanisms Induced byInternational journal of molecular sciences · 2024Review
- Immunologic features of nontuberculous mycobacterial pulmonary disease based on spatially resolved whole transcriptomics.BMC pulmonary medicine · 2024Article
- Effect and Mechanism of Mycobacterium avium MAV-5183 on Apoptosis of Mouse Ana-1 Macrophages.Cell biochemistry and biophysics · 2024Article
- Differential Immune Responses and Underlying Mechanisms of Metabolic Reprogramming in Smooth and Rough Variants ofPathogens (Basel, Switzerland) · 2023Article
- Ohmyungsamycin promotes M1-like inflammatory responses to enhance host defence againstVirulence · 2022Article
- Anti-TNF Therapies Suppress Adipose Tissue Inflammation in Crohn's Disease.International journal of molecular sciences · 2022Article
- Comparison of Macrophage Immune Responses and Metabolic Reprogramming in Smooth and Rough Variant Infections ofInternational journal of molecular sciences · 2022Article
- Host-Pathogen Interactions Operative duringImmune network · 2021Review
- Progress of the Art of Macrophage Polarization and Different Subtypes in Mycobacterial Infection.Frontiers in immunology · 2021Review
- Catalpol Inhibits Macrophage Polarization and Prevents Postmenopausal Atherosclerosis Through Regulating Estrogen Receptor Alpha.Frontiers in pharmacology · 2021Article
- Substrate stiffness modulates bone marrow-derived macrophage polarization through NF-κB signaling pathway.Bioactive materials · 2020Article
- Biological Functions of HMGN Chromosomal Proteins.International journal of molecular sciences · 2020Review
- HMGN2 regulates non-tuberculous mycobacteria survival via modulation of M1 macrophage polarization.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-tuberculous mycobacteria (NTM), also known as an environmental and atypical mycobacteria, can cause the chronic pulmonary infectious diseases. Macrophages have been suggested as the main host cell to initiate the innate immune responses to NTM infection. However, the molecular mechanism to regulate the antimicrobial immune responses to NTM is still largely unknown. Current study showed that the NTM clinical groups, Mycobacterium abscessus and Mycobacterium smegmatis, significantly induced the M1 macrophage polarization with the characteristic production of nitric oxide (NO) and marker gene expression of iNOS, IFNγ, TNF-α, IL1-β and IL-6. Interestingly, a non-histone nuclear protein, HMGN2 (high-mobility group N2), was found to be spontaneously induced during NTM-activated M1 macrophage polarization. Functional studies revealed that HMGN2 deficiency in NTM-infected macrophage promotes the expression of M1 markers and the production of NO via the enhanced activation of NF-κB and MAPK signalling. Further studies exhibited that HMGN2 knock-down also enhanced IFNγ-induced M1 macrophage polarization. Finally, we observed that silencing HMGN2 affected the survival of NTM in macrophage, which might largely relevant to enhanced macrophage polarization into M1 phenotype under the NTM infection. Collectively, current studies thus suggested a novel function of HMGN2 in regulating the anti-non-tuberculous mycobacteria innate immunity of macrophage.
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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.