ArticleCommunications biology2024
Nitric oxide induces the distinct invisibility phenotype of Mycobacterium tuberculosis.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- NRF2-mediated inhibition of alveolar macrophage MHC II expression during Mycobacterium tuberculosis infection.Cell reports · 2026Article
- Plasma protein signatures altered before and after tuberculosis diagnosis in a population-based cohort.Clinical proteomics · 2026Article
- Unexpected detection of Mycobacterium tuberculosis DNA in US-born patients in putative association with clinical syndromes.Nature communications · 2026Observational
- Impact of L-arginine and L-citrulline supplementation on macrophage responses toFrontiers in immunology · 2026Article
- Case Report: Management challenges of active tuberculosis complicated by thrombocytosis and squamous cell lung carcinoma.Frontiers in oncology · 2026Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
During infection Mycobacterium tuberculosis (Mtb) forms physiologically distinct subpopulations that are recalcitrant to treatment and undetectable using standard diagnostics. These difficult to culture or differentially culturable (DC) Mtb are revealed in liquid media, their revival is often stimulated by resuscitation-promoting factors (Rpf) and prevented by Rpf inhibitors. Here, we investigated the role of nitric oxide (NO) in promoting the DC phenotype. Rpf-dependent DC Mtb were detected following infection of interferon-γ-induced macrophages capable of producing NO, but not when inducible NO synthase was inactivated. After exposure of Mtb to a new donor for sustained NO release (named NOD), the majority of viable cells were Rpf-dependent and undetectable on solid media. Gene expression analyses revealed a broad transcriptional response to NOD, including down-regulation of all five rpf genes. The DC phenotype was partially reverted by over-expression of Rpfs which promoted peptidoglycan remodelling. Thus, NO plays a central role in the generation of Rpf-dependent Mtb, with implications for improving tuberculosis diagnostics and treatments.
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Registered trials
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