ArticlePloS one2014
Role of TNF in the altered interaction of dormant Mycobacterium tuberculosis with host macrophages.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Kicking sleepers out of bed: Macrophages promote reactivation of dormant Cryptococcus neoformans by extracellular vesicle release and non-lytic exocytosis.PLoS pathogens · 2023Article
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- Tuberculosis: The success tale of less explored dormantFrontiers in cellular and infection microbiology · 2022Review
- In-depth systems biological evaluation of bovine alveolar macrophages suggests novel insights into molecular mechanisms underlyingFrontiers in microbiology · 2022Article
- Insights into the molecular determinants involved inVirulence · 2021Review
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- Stabilization of Hypoxia-Inducible Factor Promotes Antimicrobial Activity of Human Macrophages AgainstFrontiers in immunology · 2021Article
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- In vivo inhibition of tryptophan catabolism reorganizes the tuberculoma and augments immune-mediated control ofProceedings of the National Academy of Sciences of the United States of America · 2018Article
- KillingMicrobiology spectrum · 2017Review
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- Hypoxia promotes Mycobacterium tuberculosis-specific up-regulation of granulysin in human T cells.Medical microbiology and immunology · 2016Article
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- Gene expression and TB pathogenesis in rhesus macaques: TR4, CD40, CD40L, FAS (CD95), and TNF are host genetic markers in peripheral blood mononuclear cells that are associated with severity of TB lesions.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2015Article
- DosS Is required for the complete virulence of mycobacterium tuberculosis in mice with classical granulomatous lesions.American journal of respiratory cell and molecular biology · 2015Article
- The DosR Regulon Modulates Adaptive Immunity and Is Essential for Mycobacterium tuberculosis Persistence.American journal of respiratory and critical care medicine · 2015Article
- The Mycobacterium tuberculosis Clp gene regulator is required for in vitro reactivation from hypoxia-induced dormancy.The Journal of biological chemistry · 2015Article
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Mycobacterium tuberculosis (Mtb) persists within lung granulomas, despite being subjected to diverse stress conditions, including hypoxia. We hypothesized that the response of host phagocytes to Mtb experiencing hypoxia is radically altered and designed in vitro experiment to study this phenomenon. Hypoxia-stressed (Mtb-H) and aerobically grown Mtb (Mtb-A) were used to infect Rhesus Macaque Bone Marrow Derived Macrophages (Rh-BMDMs) and the comparative host response to Mtb infection studied. Mechanistic insights were gained by employing RNAi. Mtb-H accumulated significantly lower bacterial burden during growth in Rh-BMDMs, concomitantly generating a drastically different host transcriptional profile (with only <2% of all genes perturbed by either infection being shared between the two groups). A key component of this signature was significantly higher TNF and apopotosis in Mtb-H- compared to Mtb-A-infected Rh-BMDMs. Silencing of TNF by RNAi reversed the significant control of Mtb replication. These results indicate a potential mechanism for the rapid clearance of hypoxia-conditioned bacilli by phagocytes. In conclusion, hypoxia-conditioned Mtb undergo significantly different interactions with host macrophages compared to Mtb grown in normoxia. These interactions result in the induction of the TNF signaling pathway, activation of apoptosis, and DNA-damage stress response. Our results show that Mtb-H bacilli are particularly susceptible to killing governed by TNF.
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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.