ArticlePloS one2012
Attenuated Mycobacterium tuberculosis SO2 vaccine candidate is unable to induce cell death.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
The trial behind it
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
20 citing papers in PubMed, 34 citations in OpenAlex.
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- Dual oxidase 1 is dispensable duringFrontiers in immunology · 2023Article
- Necroptotic signaling is primed in Mycobacterium tuberculosis-infected macrophages, but its pathophysiological consequence in disease is restricted.Cell death and differentiation · 2018Article
- Mycobacterium tuberculosis: Rewiring host cell signaling to promote infection.Journal of leukocyte biology · 2018Review
- Multiparametric analysis of anti-proliferative and apoptotic effects of gold nanoprisms on mouse and human primary and transformed cells, biodistribution and toxicity in vivo.Particle and fibre toxicology · 2017Article
- Asymmetric Structure of the Dimerization Domain of PhoR, a Sensor Kinase Important for the Virulence ofACS omega · 2017Article
- Strategies to Improve Vaccine Efficacy against Tuberculosis by Targeting Innate Immunity.Frontiers in immunology · 2017Review
- Mycobacterium avium MAV2054 protein induces macrophage apoptosis by targeting mitochondria and reduces intracellular bacterial growth.Scientific reports · 2016Article
- Toll-Like Receptors 2 and 4 Cooperate in the Control of the Emerging PathogenFrontiers in cellular and infection microbiology · 2016Article
- A High-Throughput Assay for Developing Inhibitors of PhoP, a Virulence Factor of Mycobacterium tuberculosis.Combinatorial chemistry & high throughput screening · 2016Article
- Tuberculosis vaccine types and timings.Clinical and vaccine immunology : CVI · 2015Review
- Duality of lipid mediators in host response against Mycobacterium tuberculosis: good cop, bad cop.F1000prime reports · 2015Review
- IL-17A Promotes Intracellular Growth of Mycobacterium by Inhibiting Apoptosis of Infected Macrophages.Frontiers in immunology · 2015Article
- DNA consensus sequence motif for binding response regulator PhoP, a virulence regulator of Mycobacterium tuberculosis.Biochemistry · 2014Article
- Bim is a crucial regulator of apoptosis induced by Mycobacterium tuberculosis.Cell death & disease · 2014Article
- Article
- ESX-1-induced apoptosis during mycobacterial infection: to be or not to be, that is the question.Frontiers in cellular and infection microbiology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been proposed that Mycobacterium tuberculosis virulent strains inhibit apoptosis and trigger cell death by necrosis of host macrophages to evade innate immunity, while non-virulent strains induce typical apoptosis activating a protective host response. As part of the characterization of a novel tuberculosis vaccine candidate, the M. tuberculosis phoP mutant SO2, we sought to evaluate its potential to induce host cell death. The parental M. tuberculosis MT103 strain and the current vaccine against tuberculosis Bacillus Calmette-Guérin (BCG) were used as comparators in mouse models in vitro and in vivo. Our data reveal that attenuated SO2 was unable to induce apoptotic events neither in mouse macrophages in vitro nor during lung infection in vivo. In contrast, virulent MT103 triggers typical apoptotic events with phosphatidylserine exposure, caspase-3 activation and nuclear condensation and fragmentation. BCG strain behaved like SO2 and did not induce apoptosis. A clonogenic survival assay confirmed that viability of BCG- or SO2-infected macrophages was unaffected. Our results discard apoptosis as the protective mechanism induced by SO2 vaccine and provide evidence for positive correlation between classical apoptosis induction and virulent strains, suggesting apoptosis as a possible virulence determinant during M. tuberculosis infection.
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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.