ArticleThe American journal of pathology2014
Bone marrow mesenchymal stem cells provide an antibiotic-protective niche for persistent viable Mycobacterium tuberculosis that survive antibiotic treatment.
Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 56 citations in OpenAlex.
- Bi-directional highways and super-seeder tissues underpin parasite dissemination in experimental Leishmania donovani infection.Nature communications · 2026Article
- Review
- The lung tissue environment inbioRxiv : the preprint server for biology · 2026Article
- Development of a score derived from full blood count parameters to differentiate individuals with tuberculosis disease from those with tuberculosis infection.Clinical and experimental immunology · 2026Article
- Common Adverse Reactions and Management Strategies of First-Line Anti-Tuberculosis Drugs.Infection and drug resistance · 2026Review
- The Impact of Animal Models and Strain Standardization on the Evaluation of Tuberculosis Vaccine Efficacy.Vaccines · 2025Review
- Global proteomics reveals pathways of mesenchymal stem cells altered by Mycobacterium tuberculosis.Scientific reports · 2024Article
- Long-term hematopoietic stem cells trigger quiescence in Leishmania parasites.PLoS pathogens · 2024Article
- Article
- Detection of Mycobacterial DNA in Human Bone Marrow.Microorganisms · 2023Article
- Revisiting the role of mesenchymal stem cells in tuberculosis and other infectious diseases.Cellular & molecular immunology · 2023Review
- Serum amyloid A proteins reduce bone mass during mycobacterial infections.Frontiers in immunology · 2023Article
- Long-term hematopoietic stem cells as a parasite niche during treatment failure in visceral leishmaniasis.Communications biology · 2022Article
- Observational
- Cumulative Signaling Through NOD-2 and TLR-4 Eliminates theFrontiers in cellular and infection microbiology · 2021Article
- Human mesenchymal stem cell based intracellular dormancy model of Mycobacterium tuberculosis.Microbes and infection · 2020Article
- Mesenchymal stem cells offer a drug-tolerant and immune-privileged niche to Mycobacterium tuberculosis.Nature communications · 2020Article
- Preclinical Evidence of Nanomedicine Formulation to TargetPathogens (Basel, Switzerland) · 2020Article
- Mycobacterium tuberculosis programs mesenchymal stem cells to establish dormancy and persistence.The Journal of clinical investigation · 2020Article
- Anatomic and Cellular Niches for Mycobacterium tuberculosis in Latent Tuberculosis Infection.The Journal of infectious diseases · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
During tuberculosis (TB), some Mycobacterium tuberculosis bacilli persist in the presence of an active immunity and antibiotics that are used to treat the disease. Herein, by using the Cornell model of TB persistence, we further explored our recent finding that suggested that M. tuberculosis can escape therapy by residing in the bone marrow (BM) mesenchymal stem cells. We initially showed that M. tuberculosis rapidly disseminates to the mouse BM after aerosol exposure and maintained a stable burden for at least 220 days. In contrast, in the lungs, the M. tuberculosis burden peaked at 28 days and subsequently declined approximately 10-fold. More important, treatment of the mice with the antibiotics rifampicin and isoniazid, as expected, resulted in effective clearance of M. tuberculosis from the lungs and spleen. In contrast, M. tuberculosis persisted, albeit at low numbers, in the BM of antibiotic-treated mice. Moreover, most viable M. tuberculosis was recovered from the bone marrow CD271(+)CD45(-)-enriched cell fraction, and only few viable bacteria could be isolated from the CD271(-)CD45(+) cell fraction. These results clearly show that BM mesenchymal stem cells provide an antibiotic-protective niche for M. tuberculosis and suggest that unraveling the mechanisms underlying this phenomenon will enhance our understanding of M. tuberculosis persistence in treated TB patients.
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