ArticleInfection and immunity2009
Protection of Mycobacterium tuberculosis from reactive oxygen species conferred by the mel2 locus impacts persistence and dissemination.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
38 citing papers in PubMed, 67 citations in OpenAlex.
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- The inflammasome adaptor pycard is essential for immunity against Mycobacterium marinum infection in adult zebrafish.Disease models & mechanisms · 2025Article
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- EphH, a unique epoxide hydrolase encoded by Rv3338 is involved in the survival ofFrontiers in microbiology · 2022Article
- Cellular Self-Digestion and Persistence in Bacteria.Microorganisms · 2021Review
- Targeting Molecular Inflammatory Pathways in Granuloma as Host-Directed Therapies for Tuberculosis.Frontiers in immunology · 2021Review
- Monitoring Persister Resuscitation with Flow Cytometry.Methods in molecular biology (Clifton, N.J.) · 2021Article
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- Diagnostic host gene signature for distinguishing enteric fever from other febrile diseases.EMBO molecular medicine · 2019Article
- Mce3R Stress-Resistance Pathway Is Vulnerable to Small-Molecule Targeting That Improves Tuberculosis Drug Activities.ACS infectious diseases · 2019Article
- Evaluation of in silico designed inhibitors targeting MelF (Rv1936) against Mycobacterium marinum within macrophages.Scientific reports · 2019Article
- More than cholesterol catabolism: regulatory vulnerabilities in Mycobacterium tuberculosis.Current opinion in chemical biology · 2018Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Persistence of Mycobacterium tuberculosis in humans represents a major roadblock to elimination of tuberculosis. We describe identification of a locus in M. tuberculosis, mel2, that displays similarity to bacterial bioluminescent loci and plays an important role during persistence in mice. We constructed a deletion of the mel2 locus and found that the mutant displays increased susceptibility to reactive oxygen species (ROS). Upon infection of mice by aerosol the mutant grows normally until the persistent stage, where it does not persist as well as wild type. Histopathological analyses show that infection with the mel2 mutant results in reduced pathology and both CFU and histopathology indicate that dissemination of the mel2 mutant to the spleen is delayed. These data along with growth in activated macrophages and infection of Phox(-/-) and iNOS(-/-) mice and bone marrow-derived macrophages suggest that the primary mechanism by which mel2 affects pathogenesis is through its ability to confer resistance to ROS. These studies provide the first insight into the mechanism of action for this novel class of genes that are related to bioluminescence genes. The role of mel2 in resistance to ROS is important for persistence and dissemination of M. tuberculosis and suggests that homologues in other bacterial species are likely to play a role in pathogenesis.
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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.