ArticlePloS one2009
Voltage gated calcium channels negatively regulate protective immunity to Mycobacterium tuberculosis.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Effect of calcium-channel blockers on the risk of active tuberculosis and mortality: systematic review and meta-analysis.Frontiers in pharmacology · 2024Pooled it
- Reversion of a RND transporter pseudogene reveals latent stress resistance potential in Brucella ovis.PLoS genetics · 2025Article
- Exploring a Rare Association: Systematic Review of Hypercalcemia in Nontuberculous Mycobacterial Infections.Microorganisms · 2025Review
- Genome-wide association study of tuberculosis in the western Chinese Han and Tibetan population.MedComm · 2023Article
- Mycobacteria modulate SUMOylation to suppresses protective responses in dendritic cells.PloS one · 2023Article
- The Impact of Hypertension and Use of Calcium Channel Blockers on Tuberculosis Treatment Outcomes.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2021Article
- MIDESP: Mutual Information-Based Detection of Epistatic SNP Pairs for Qualitative and Quantitative Phenotypes.Biology · 2021Article
- Review
- Expression ofCentral-European journal of immunology · 2021Article
- Targeting microglia L-type voltage-dependent calcium channels for the treatment of central nervous system disorders.Journal of neuroscience research · 2021Review
- Something Old, Something New: Ion Channel Blockers as Potential Anti-Tuberculosis Agents.Frontiers in immunology · 2021Review
- Ion Transport Modulators Differentially Modulate Inflammatory Responses in THP-1-Derived Macrophages.Journal of immunology research · 2021Article
- The Use of Pulsed Electromagnetic Field to Modulate Inflammation and Improve Tissue Regeneration: A Review.Bioelectricity · 2019Review
- Blocking αFrontiers in pharmacology · 2019Article
- Meta-analysis of human gene expression in response to Mycobacterium tuberculosis infection reveals potential therapeutic targets.BMC systems biology · 2018Article
- Bacterial subversion of cAMP signalling inhibits cathelicidin expression, which is required for innate resistance to Mycobacterium tuberculosis.The Journal of pathology · 2017Article
- Thioridazine: A Non-Antibiotic Drug Highly Effective, in Combination with First Line Anti-Tuberculosis Drugs, against Any Form of Antibiotic Resistance of Mycobacterium tuberculosis Due to Its Multi-Mechanisms of Action.Antibiotics (Basel, Switzerland) · 2017Review
- Novel cell-based in vitro screen to identify small-molecule inhibitors against intracellular replication of Cryptococcus neoformans in macrophages.International journal of antimicrobial agents · 2016Article
- Bioelectric modulation of macrophage polarization.Scientific reports · 2016Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium tuberculosis modulates levels and activity of key intracellular second messengers to evade protective immune responses. Calcium release from voltage gated calcium channels (VGCC) regulates immune responses to pathogens. In this study, we investigated the roles of VGCC in regulating protective immunity to mycobacteria in vitro and in vivo. Inhibiting L-type or R-type VGCC in dendritic cells (DCs) either using antibodies or by siRNA increased calcium influx in an inositol 1,4,5-phosphate and calcium release calcium activated channel dependent mechanism that resulted in increased expression of genes favoring pro-inflammatory responses. Further, VGCC-blocked DCs activated T cells that in turn mediated killing of M. tuberculosis inside macrophages. Likewise, inhibiting VGCC in infected macrophages and PBMCs induced calcium influx, upregulated the expression of pro-inflammatory genes and resulted in enhanced killing of intracellular M. tuberculosis. Importantly, compared to healthy controls, PBMCs of tuberculosis patients expressed higher levels of both VGCC, which were significantly reduced following chemotherapy. Finally, blocking VGCC in vivo in M. tuberculosis infected mice using specific antibodies increased intracellular calcium and significantly reduced bacterial loads. These results indicate that L-type and R-type VGCC play a negative role in M. tuberculosis infection by regulating calcium mobilization in cells that determine protective immunity.
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What OpenQuestion holds
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.