ArticleThe Journal of experimental medicine2000
Inhibition of Ca(2+) signaling by Mycobacterium tuberculosis is associated with reduced phagosome-lysosome fusion and increased survival within human macrophages.
Article in The Journal of experimental medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
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Who cites it
112 citing papers in PubMed, 333 citations in OpenAlex.
- Functional single nucleotide polymorphisms in CACNA2D3 and other autophagy-related genes are associated with leprosy among Brazilians.PLoS neglected tropical diseases · 2026Article
- Intracellular Calcium as a Regulator of Polarization and Target Reprogramming of Macrophages.International journal of molecular sciences · 2025Review
- Single-cell RNA sequencing reveals immune cell dysfunction and rewired interaction networks in the peripheral blood of active tuberculosis patients.BMC immunology · 2025Article
- The host calcium system contributes to intracellularInfection and immunity · 2025Article
- Immunomodulatory activity of 4-(Benzyloxy)phenol facilitates intracellular mycobacterial clearance through p53 mediated IL-35 signaling dependent JAK1/STAT3 pathway in human macrophages.Immunologic research · 2025Article
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- High throughput screening assay for the identification of ATF4 and TFEB activating compounds.Autophagy reports · 2025Article
- Unveiling the immunological landscape of disseminated tuberculosis: a single-cell transcriptome perspective.Frontiers in immunology · 2025Article
- Iron-restricted Mycobacterium tuberculosis exports pathogenicity factors packed in extracellular vesicles.PloS one · 2025Article
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- Genome-wide screen of Mycobacterium tuberculosis-infected macrophages revealed GID/CTLH complex-mediated modulation of bacterial growth.Nature communications · 2024Article
- Extensive differential DNA methylation between tuberculosis skin test positive and skin test negative cattle.BMC genomics · 2024Article
- From pathogenesis to antigens: the key to shaping the future of TB vaccines.Frontiers in immunology · 2024Review
- Antibodies as key mediators of protection againstFrontiers in immunology · 2024Review
- Evolution of Hematobiochemical Profiles in Newly Diagnosed HIV Patients and HIV-TB Co-Infected Patients: Correlation with Immunological and Virological Status.ImmunoTargets and therapy · 2024Article
- Macrophages, Metabolism, Mitochondria, Circadian Rhythmicity and the Pathogen: The Multidimensional Nature of Tuberculosis.Results and problems in cell differentiation · 2024Review
- Mycobacterium tuberculosis and its clever approaches to escape the deadly macrophage.World journal of microbiology & biotechnology · 2023Review
- Discovery of Novel Transketolase Epitopes and the Development of IgG-Based Tuberculosis Serodiagnostics.Microbiology spectrum · 2023Article
- Host-directed therapy against tuberculosis: Concept and recent developments.Journal of biosciences · 2023Review
- TWEAK-Fn14 Axis Induces Calcium-Associated Autophagy and Cell Death To Control Mycobacterial Survival in Macrophages.Microbiology spectrum · 2022Article
52 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Complement receptor (CR)-mediated phagocytosis of Mycobacterium tuberculosis by macrophages results in intracellular survival, suggesting that M. tuberculosis interferes with macrophage microbicidal mechanisms. As increases in cytosolic Ca(2+) concentration (¿Ca(2+)(c)) promote phagocyte antimicrobial responses, we hypothesized that CR phagocytosis of M. tuberculosis is accompanied by altered Ca(2+) signaling. Whereas the control complement (C)-opsonized particle zymosan (COZ) induced a 4.6-fold increase in ¿Ca(2+)(c) in human macrophages, no change in ¿Ca(2+)(c) occurred upon addition of live, C-opsonized virulent M. tuberculosis. Viability of M. tuberculosis and ingestion via CRs was required for infection of macrophages in the absence of increased ¿Ca(2+)(c), as killed M. tuberculosis or antibody (Ab)-opsonized, live M. tuberculosis induced elevations in ¿Ca(2+)(c) similar to COZ. Increased ¿Ca(2+)(c) induced by Ab-opsonized bacilli was associated with a 76% reduction in intracellular survival, compared with C-opsonized M. tuberculosis. Similarly, reversible elevation of macrophage ¿Ca(2+)(c) with the ionophore A23187 reduced intracellular viability by 50%. Ionophore-mediated elevation of ¿Ca(2+)(c) promoted the maturation of phagosomes containing live C-opsonized bacilli, as evidenced by acidification and accumulation of lysosomal protein markers. These data demonstrate that M. tuberculosis inhibits CR-mediated Ca(2+) signaling and indicate that this alteration of macrophage activation contributes to inhibition of phagosome-lysosome fusion and promotion of intracellular mycobacterial survival.
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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.