ArticleBMC microbiology2014
Mycobacterium tuberculosis expressing phospholipase C subverts PGE2 synthesis and induces necrosis in alveolar macrophages.
Article in BMC microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
- Host-strain compatibility shapes host transcriptional responses in macrophageMicrobial genomics · 2026Article
- Interred mechanisms of resistance and host immune evasion revealed through network-connectivity analysis ofmSystems · 2025Article
- D609 Suppresses Antituberculosis Response by Regulating Dendritic Cells Antigen Presentation.Immunity, inflammation and disease · 2024Article
- Immunoinformatics and structural aided approach to develop multi-epitope based subunit vaccine against Mycobacterium tuberculosis.Scientific reports · 2024Article
- Phospholipase C epsilon-1 (PLCƐ1) mediates macrophage activation and protection against tuberculosis.Infection and immunity · 2024Article
- Phospholipase C: underrated players in microbial infections.Frontiers in cellular and infection microbiology · 2023Review
- Modulatory Impact of the sRNA Mcr11 in Two Clinical Isolates of Mycobacterium tuberculosis.Current microbiology · 2022Article
- Functional Analysis of Hypothetical Proteins ofBioinformatics and biology insights · 2022Article
- Latent tuberculosis: interaction of virulence factors in Mycobacterium tuberculosis.Molecular biology reports · 2021Review
- MicroRNA-155 Modulates Macrophages' Response to Non-Tuberculous Mycobacteria through COX-2/PGE2 Signaling.Pathogens (Basel, Switzerland) · 2021Article
- Competitive Cell Death Interactions in Pulmonary Infection: Host Modulation Versus Pathogen Manipulation.Frontiers in immunology · 2020Review
- Prostaglandin EPharmacology & therapeutics · 2018Review
- Prostaglandins DJournal of lipid research · 2018Article
- Leukotriene BScientific reports · 2017Article
- Morphoproteomic-Guided Host-Directed Therapy for Tuberculosis.Frontiers in immunology · 2017Article
- Deciphering the virulence factors of the opportunistic pathogenNew microbes and new infections · 2016Article
- Mycobacterium tuberculosis PPE68 and Rv2626c genes contribute to the host cell necrosis and bacterial escape from macrophages.Virulence · 2016Article
- ISMapper: identifying transposase insertion sites in bacterial genomes from short read sequence data.BMC genomics · 2015Article
- Cytokine and lipid mediator networks in tuberculosis.Immunological reviews · 2015Review
- DNA damage and cellular abnormalities in tuberculosis, lung cancer and chronic obstructive pulmonary disease.Multidisciplinary respiratory medicine · 2015Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPhospholipases C (PLCs) are virulence factors found in several bacteria. In Mycobacterium tuberculosis (Mtb) they exhibit cytotoxic effects on macrophages, but the mechanisms involved in PLC-induced cell death are not fully understood. It has been reported that induction of cell necrosis by virulent Mtb is coordinated by subversion of PGE2, an essential factor in cell membrane protection.
resultsUsing two Mtb clinical isolates carrying genetic variations in PLC genes, we show that the isolate 97-1505, which bears plcA and plcB genes, is more resistant to alveolar macrophage microbicidal activity than the isolate 97-1200, which has all PLC genes deleted. The isolate 97-1505 also induced higher rates of alveolar macrophage necrosis, and likewise inhibited COX-2 expression and PGE2 production. To address the direct effect of mycobacterial PLC on cell necrosis and PGE2 inhibition, both isolates were treated with PLC inhibitors prior to macrophage infection. Interestingly, inhibition of PLCs affected the ability of the isolate 97-1505 to induce necrosis, leading to cell death rates similar to those induced by the isolate 97-1200. Finally, PGE2 production by Mtb 97-1505-infected macrophages was restored to levels similar to those produced by 97-1200-infected cells.
conclusionsMycobacterium tuberculosis bearing PLCs genes induces alveolar macrophage necrosis, which is associated to subversion of PGE2 production.
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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.