ArticlePloS one2015
The Role of High Mobility Group Box 1 Protein (HMGB1) in the Immunopathology of Experimental Pulmonary Tuberculosis.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Unlocking the Diagnostic Challenge of Tuberculosis and Sarcoidosis Intrathoracic Lymphadenopathy: Potential Role of HMGB1 and miRNA-221 as Diagnostic Tools.Microorganisms · 2026Article
- Assessing the inflammation in pediatric MOGAD: Significance of CSF HMGB1 and related biomarkers.Frontiers in immunology · 2025Article
- Protein dysregulation duringFrontiers in immunology · 2025Article
- Decoding the hidden realm: Molecular pioneering unravelling osteoarticular tuberculosis diagnosis.Journal of clinical orthopaedics and trauma · 2024Article
- The multifunctional protein HMGB1: 50 years of discovery.Nature reviews. Immunology · 2023Review
- Article
- The Role of HMGB1, a Nuclear Damage-Associated Molecular Pattern Molecule, in the Pathogenesis of Lung Diseases.Antioxidants & redox signaling · 2019Review
- International collaboration among medical societies is an effective way to boost Latin American production of articles on tuberculosis.Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia · 2019Article
- Lipoxin A4 and its analog suppress inflammation by modulating HMGB1 translocation and expression in psoriasis.Scientific reports · 2017Article
- Down-Regulation of Serum High-Mobility Group Box 1 Protein in Patients with Pulmonary Tuberculosis and Nontuberculous Mycobacterial Lung Disease.Tuberculosis and respiratory diseases · 2017Article
- Trypanosoma cruzi High Mobility Group B (TcHMGB) can act as an inflammatory mediator on mammalian cells.PLoS neglected tropical diseases · 2017Article
- HMGB1/RAGE Signaling and Pro-Inflammatory Cytokine Responses in Non-HIV Adults with Active Pulmonary Tuberculosis.PloS one · 2016Article
- Immune Cell Regulatory Pathways Unexplored as Host-Directed Therapeutic Targets for Mycobacterium tuberculosis: An Opportunity to Apply Precision Medicine Innovations to Infectious Diseases.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2015Review
- Correction: The Role of High Mobility Group Box 1 Protein (HMGB1) in the Immunopathology of Experimental Pulmonary Tuberculosis.PloS one · 2015Article
Corrections and comments
- Erratum issuedCorrection: The Role of High Mobility Group Box 1 Protein (HMGB1) in the Immunopathology of Experimental Pulmonary Tuberculosis.2015 · Botasso, Oscar Adelmo [corrected to Bottasso, Oscar Adelmo]
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe high mobility group box 1 (HMGB1) is the prototype of alarmin protein released by stressed or dying cells. The redox state of this protein confers different functions in the regulation of inflammation and immune response.
aimDetermine the kinetics, cellular sources and function of HMGB1 in experimental tuberculosis.
methodsBALB/c mice were infected with Mycobacterium tuberculosis strain H37Rv. At different time points, HMGB1 was quantified in bronchial lavage fluid (BALF) and in lungs was determined its cellular sources by immunohistochemistry. HMGB1 was blocked with specific antibodies or recombinant HMGB1 was administered during early or late infection. Bacilli burdens, inflammation and cytokines expression were determined.
resultsThe maximal concentration of HMGB1 in BALF was at day one of infection. Bronchial epithelium and macrophages were the most important sources. At day 7 to 21 the oxidized HMGB1 was predominant, while during late infection only the reduced form was seen. Blocking HMGB1 during early infection produced significant decrease of bacilli burdens and high production of pro-inflammatory cytokines, while the opposite was seen when HMGB1 was administered. Blocking HMGB1 activity or administrated it in high amounts during late infection worsening the disease.
conclusionsHMGB1 is liberated during experimental tuberculosis and promotes or suppress the immune response and inflammation depending on the redox state.
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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.