ArticleRedox biology2015
Induction of heme oxygenase-1 contributes to survival of Mycobacterium abscessus in human macrophages-like THP-1 cells.
Article in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 58 citations in OpenAlex.
- Punicalagin Enhances Autophagy Through Sirtuin 1/FoxO3a Axis to Inhibit Intracellular Mycobacterium Abscessus Infection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Ouabain alleviatesFrontiers in immunology · 2025Article
- Heme Oxygenase-1 and Prostate Cancer: Function, Regulation, and Implication in Cancer Therapy.International journal of molecular sciences · 2024Review
- Understanding the development of tuberculous granulomas: insights into host protection and pathogenesis, a review in humans and animals.Frontiers in immunology · 2024Review
- Isoegomaketone exhibits potential as a newFrontiers in microbiology · 2024Article
- Molecular Identification of Strains within thePolish journal of microbiology · 2023Article
- Modulation of Heme-Induced Inflammation Using MicroRNA-Loaded Liposomes: Implications for Hemolytic Disorders Such as Malaria and Sickle Cell Disease.International journal of molecular sciences · 2023Article
- Druggable redox pathways against Mycobacterium abscessus in cystic fibrosis patient-derived airway organoids.PLoS pathogens · 2023Article
- The pathogenicity and virulence of Leishmania - interplay of virulence factors with host defenses.Virulence · 2022Review
- Heme Oxygenase/Carbon Monoxide Participates in the Regulation ofInternational journal of molecular sciences · 2022Article
- A Dual Role of Heme Oxygenase-1 in Tuberculosis.Frontiers in immunology · 2022Review
- Heme-Oxygenase-1 Attenuates Oxidative Functions of Antigen Presenting Cells and Promotes Regulatory T Cell Differentiation duringAntioxidants (Basel, Switzerland) · 2021Article
- Pathomechanisms of Immunological Disturbances in β-Thalassemia.International journal of molecular sciences · 2021Review
- Nrf2 Activation Attenuates Acrylamide-Induced Neuropathy in Mice.International journal of molecular sciences · 2021Article
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- Heme Oxygenase-1 Signaling and Redox Homeostasis in Physiopathological Conditions.Biomolecules · 2021Review
- Heme Oxygenase-1 as a Pharmacological Target for Host-Directed Therapy to Limit Tuberculosis Associated Immunopathology.Antioxidants (Basel, Switzerland) · 2021Review
- Progress of the Art of Macrophage Polarization and Different Subtypes in Mycobacterial Infection.Frontiers in immunology · 2021Review
- Heme oxygenase-1 inhibition promotes IFNγ- and NOS2-mediated control of Mycobacterium tuberculosis infection.Mucosal immunology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mycobacterium abscessus (M.abs) is a rapidly growing mycobacterial species that infects macrophages, and is an important pathogen in patients with cystic fibrosis. We studied the early stages of M.abs infection of macrophages, with emphasis on the role of heme-oxygenase-1 (HO-1) in this infection. THP-1 cells were activated using TPA into macrophage-like cells and infected with M.abs for different time points. M.abs infection robustly induced HO-1 expression in the THP-1 cells. Production of HO-1 was p38 MAPK-dependent, as p38 inhibitors suppressed HO-1 induction. Pretreatment with HO-1 inhibitors tin-protoporphyrin (SnPP) significantly inhibited M.abs growth inside macrophages. Furthermore, inhibiting HO-1 using HO-1 siRNA or the HO-1 upstream signaling molecule; Nrf2 using Nrf2 siRNA resulted in similar inhibition of M.abs. In contrast, inducing HO-1 did not increase M.abs intracellular growth above control. Products of HO-1 metabolism of heme are bilirubin, biliverdin, carbon monoxide (CO) and iron. The addition of either bilirubin or biliverdin, but not CO, completely restored the SnPP inhibitory effect and partially that with HO-1 siRNA. To understand the mechanisms, we used Syto-62 labeled M.abs to infect macrophages. Interestingly, HO-1 inhibition promoted M.abs-containing phagosome fusion with lysosomes, which should enhance M.abs killing. M.abs infection enhanced THP-1 ROS production as demonstrated by increased DHE, DCF fluorescence, and EPR signal. HO-1 inhibition further increased ROS production in infected macrophages. Our results indicate that HO-1 induction is important for M.abs growth during the early stages of infection, and that the HO-1 products bilirubin and biliverdin, perhaps through modulation of intracellular ROS levels, may be involved.
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