ArticleInfection and immunity2001
Cu,Zn superoxide dismutase of Mycobacterium tuberculosis contributes to survival in activated macrophages that are generating an oxidative burst.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.
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Who cites it
121 citing papers in PubMed, 289 citations in OpenAlex.
- A copper uptake ABC transport system is essential forEmerging microbes & infections · 2026Article
- Pathogenesis of Tuberculosis: Interplay Between Host Antituberculosis Immunity and Immune Evasion Strategies ofMedComm · 2026Review
- Oxidative modifications of tuberculosis antigen Ag85B alter its T cell antigenicity.Redox biology · 2026Article
- Stage-associated enrichment ofFrontiers in veterinary science · 2026Article
- To establish an indirect ELISA method for the detection of human brucellosis based on signal peptide-truncated recombinant Cu/Zn SOD and its preliminary clinical verification.Frontiers in cellular and infection microbiology · 2026Article
- Protein-Mediated Virulence in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Review
- Structural Studies on the M. tuberculosis Nucleoid-associated-Protein, NapA, Indicates DNA Bridging Mechanism.Journal of molecular biology · 2025Article
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- Dissecting antimicrobial logic: species-specific strategies for intracellular pathogen defense.mSphere · 2025Review
- Review of BCG immunotherapy for bladder cancer.Clinical microbiology reviews · 2025Review
- Cu2+ mediates the oxidation of the transcription factor MscA to regulate the antioxidant defense of mycobacteria.Nucleic acids research · 2025Article
- Copper homeostasis; A rapier between mycobacteria and macrophages.FASEB bioAdvances · 2025Review
- Long-range charge transfer mechanism of the IIINature communications · 2024Article
- Live Attenuated Vaccines against Tuberculosis: Targeting the Disruption of Genes Encoding the Secretory Proteins of Mycobacteria.Vaccines · 2024Review
- The Benefits of Toxicity:Microorganisms · 2023Article
- Host hydrocarbons protect symbiont transmission from a radical host defense.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Mycobacterium tuberculosis Rv1324 Protein Contributes to Mycobacterial Persistence and Causes Pathological Lung Injury in Mice by Inducing Ferroptosis.Microbiology spectrum · 2023Article
- Targeted Mutagenesis of Mycobacterium Strains by Homologous Recombination.Methods in molecular biology (Clifton, N.J.) · 2023Article
- HEmerging microbes & infections · 2022Article
- Short-Term Exposure to MPs and DEHP Disrupted Gill Functions in Marine Bivalves.Nanomaterials (Basel, Switzerland) · 2022Article
61 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Macrophages produce reactive oxygen species and reactive nitrogen species that have potent antimicrobial activity. Resistance to killing by macrophages is critical to the virulence of Mycobacterium tuberculosis. M. tuberculosis has two genes encoding superoxide dismutase proteins, sodA and sodC. SodC is a Cu,Zn superoxide dismutase responsible for only a minor portion of the superoxide dismutase activity of M. tuberculosis. However, SodC has a lipoprotein binding motif, which suggests that it may be anchored in the membrane to protect M. tuberculosis from reactive oxygen intermediates at the bacterial surface. To examine the role of the Cu,Zn superoxide dismutase in protecting M. tuberculosis from the toxic effects of exogenously generated reactive oxygen species, we constructed a null mutation in the sodC gene. In this report, we show that the M. tuberculosis sodC mutant is readily killed by superoxide generated externally, while the isogenic parental M. tuberculosis is unaffected under these conditions. Furthermore, the sodC mutant has enhanced susceptibility to killing by gamma interferon (IFN-gamma)-activated murine peritoneal macrophages producing oxidative burst products but is unaffected by macrophages not activated by IFN-gamma or by macrophages from respiratory burst-deficient mice. These observations establish that the Cu,Zn superoxide dismutase contributes to the resistance of M. tuberculosis against oxidative burst products generated by activated macrophages.
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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.