ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Heme Oxygenase-1 Regulates Inflammation and Mycobacterial Survival in Human Macrophages during Mycobacterium tuberculosis Infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. 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, 57 citations in OpenAlex.
- CD73Nature communications · 2026Article
- Host-directed therapeutic targets in macrophages and their ligands against mycobacteria tuberculosis.Infection and immunity · 2025Review
- Single-cell analysis revealsScience advances · 2025Article
- The heme oxygenase-1 metalloporphyrin inhibitor stannsoporfin enhances the bactericidal activity of a novel regimen for multidrug-resistant tuberculosis in a murine model.Antimicrobial agents and chemotherapy · 2024Article
- Membrane-Bound Redox Enzyme CytochromeInternational journal of molecular sciences · 2024Article
- The clinical relevance of heme detoxification by the macrophage heme oxygenase system.Frontiers in immunology · 2024Review
- The heme oxygenase-1 metalloporphyrin inhibitor stannsoporfin enhances the bactericidal activity of a novel regimen for multidrug-resistant tuberculosis in a murine model.bioRxiv : the preprint server for biology · 2023Article
- Bag it, tag it: ubiquitin ligases and host resistance to Mycobacterium tuberculosis.Trends in microbiology · 2022Review
- Increased Heme Oxygenase 1 Expression upon a Primary Exposure to the Respiratory Syncytial Virus and a SecondaryAntioxidants (Basel, Switzerland) · 2022Article
- Recent Advances in Host-Directed Therapies for Tuberculosis and Malaria.Frontiers in cellular and infection microbiology · 2022Review
- A Dual Role of Heme Oxygenase-1 in Tuberculosis.Frontiers in immunology · 2022Review
- Comparative transcriptomic analysis of THP-1-derived macrophages infected with Mycobacterium tuberculosis H37Rv, H37Ra and BCG.Journal of cellular and molecular medicine · 2021Article
- Pathomechanisms of Immunological Disturbances in β-Thalassemia.International journal of molecular sciences · 2021Review
- Regulation of inflammation by the antioxidant haem oxygenase 1.Nature reviews. Immunology · 2021Review
- Hydrogen Sulfide and Carbon Monoxide Tolerance in Bacteria.Antioxidants (Basel, Switzerland) · 2021Review
- The Ubiquitination System within Bacterial Host-Pathogen Interactions.Microorganisms · 2021Review
- Heme Oxygenase-1 as a Pharmacological Target for Host-Directed Therapy to Limit Tuberculosis Associated Immunopathology.Antioxidants (Basel, Switzerland) · 2021Review
- Heme oxygenase-1 inhibition promotes IFNγ- and NOS2-mediated control of Mycobacterium tuberculosis infection.Mucosal immunology · 2021Article
- Heme oxygenase 1 plays a crucial role in swamp eel response to oxidative stress induced by cadmium exposure or Aeromonas hydrophila infection.Fish physiology and biochemistry · 2020Article
- Modulation of Inflammation and Immune Responses by Heme Oxygenase-1: Implications for Infection with Intracellular Pathogens.Antioxidants (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Mycobacterium tuberculosis, the causative agent of tuberculosis, is responsible for 1.5 million deaths annually. We previously showed that M. tuberculosis infection in mice induces expression of the CO-producing enzyme heme oxygenase (HO1) and that CO is sensed by M. tuberculosis to initiate a dormancy program. Further, mice deficient in HO1 succumb to M. tuberculosis infection more readily than do wild-type mice. Although mouse macrophages control intracellular M. tuberculosis infection through several mechanisms, such as NO synthase, the respiratory burst, acidification, and autophagy, how human macrophages control M. tuberculosis infection remains less well understood. In this article, we show that M. tuberculosis induces and colocalizes with HO1 in both mouse and human tuberculosis lesions in vivo, and that M. tuberculosis induces and colocalizes with HO1 during primary human macrophage infection in vitro. Surprisingly, we find that chemical inhibition of HO1 both reduces inflammatory cytokine production by human macrophages and restricts intracellular growth of mycobacteria. Thus, induction of HO1 by M. tuberculosis infection may be a mycobacterial virulence mechanism to enhance inflammation and bacterial growth.
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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.