ArticleScientific reports2016
Macrophage-mediated inflammatory response decreases mycobacterial survival in mouse MSCs by augmenting NO production.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
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- A protective role for type I interferon signaling following infection with Mycobacterium tuberculosis carrying the rifampicin drug resistance-conferring RpoB mutation H445Y.PLoS pathogens · 2024Article
- Orphan response regulator NnaR is critical for nitrate and nitrite assimilation inFrontiers in cellular and infection microbiology · 2024Article
- Mitochondrial electron transport chain in macrophage reprogramming: Potential role in antibacterial immune response.Current research in immunology · 2024Review
- Can mesenchymal stem/stromal cells and their secretomes combat bacterial persisters?World journal of microbiology & biotechnology · 2023Review
- Taurine mitigates the development of pulmonary inflammation, oxidative stress, and histopathological alterations in a rat model of bile duct ligation.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- Enhanced immunogenicity of the tuberculosis subunit Rv0572c vaccine delivered in DMT liposome adjuvant as a BCG-booster.Tuberculosis (Edinburgh, Scotland) · 2022Article
- Itaconate, Arginine, and Gamma-Aminobutyric Acid: A Host Metabolite Triad Protective Against Mycobacterial Infection.Frontiers in immunology · 2022Review
- Metabolomics activity screening of T cell-induced colitis reveals anti-inflammatory metabolites.Science signaling · 2021Article
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- Potential of Mesenchymal Stem Cell-Derived Exosomes as a Novel Treatment for Female Infertility Caused by Bacterial Infections.Frontiers in microbiology · 2021Review
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- HMGN2 regulates non-tuberculous mycobacteria survival via modulation of M1 macrophage polarization.Journal of cellular and molecular medicine · 2019Article
- Anatomic and Cellular Niches for Mycobacterium tuberculosis in Latent Tuberculosis Infection.The Journal of infectious diseases · 2019Review
- Mycobacterium tuberculosis-Infected Hematopoietic Stem and Progenitor Cells Unable to Express Inducible Nitric Oxide Synthase Propagate Tuberculosis in Mice.The Journal of infectious diseases · 2018Article
- Ethyl Acetate Fraction fromEvidence-based complementary and alternative medicine : eCAM · 2018Article
- Beta-Defensin 2 and 3 Promote Bacterial Clearance ofFrontiers in immunology · 2018Article
- Guanine nucleotide exchange factor -H1 promotes inflammatory cytokine production and intracellular mycobacterial elimination in macrophages.Cell cycle (Georgetown, Tex.) · 2017Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium tuberculosis (MTB) is a hard-to-eradicate intracellular microbe, which escapes host immune attack during latent infection. Recent studies reveal that mesenchymal stem cells (MSCs) provide a protective niche for MTB to maintain latency. However, the regulation of mycobacterial residency in MSCs in the infectious microenvironment remains largely unknown. Here, we found that macrophage-mediated inflammatory response during MTB infection facilitated the clearance of bacilli residing in mouse MSCs. Higher inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) production were observed in mouse MSCs under macrophage-mediated inflammatory circumstance. Blocking NO production in MSCs increased the survival of intracellular mycobacteria, indicating NO-mediated antimycobacterial activity. Moreover, both nuclear factor κB (NF-κB) and Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathways were involved in iNOS expression and NO production in inflammatory microenvironment. Furthermore, pro-inflammatory cytokine interleukin-1β could trigger NO production in MSCs and exert anti-mycobacterial activity via NF-κB signaling pathway. Neutralization of interleukin-1β in macrophage-mediated inflammatory microenvironment dampened the ability of mouse MSCs to produce NO. Together, our findings demonstrated that macrophage-mediated inflammatory response during mycobacterial infection promotes the clearance of bacilli in mouse MSCs by increasing NO production, which may provide a better understanding of latent MTB infection.
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