ArticleInfection and immunity2006
Cytosolic phospholipase A2 enzymes are not required by mouse bone marrow-derived macrophages for the control of Mycobacterium tuberculosis in vitro.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Phospholipase A2 Isoforms in Lung Immunity and Respiratory Infections: Potential Targets for Next-Generation Therapy.International journal of molecular sciences · 2026Review
- Gram-negative bacteria-driven increase of cytosolic phospholipase A2 leads to activation of Kupffer cells.Cellular and molecular life sciences : CMLS · 2024Article
- MceG stabilizes the Mce1 and Mce4 transporters in Mycobacterium tuberculosis.The Journal of biological chemistry · 2023Article
- Growth ofProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Mycobacterial escape from macrophage phagosomes to the cytoplasm represents an alternate adaptation mechanism.Scientific reports · 2016Article
- Host-directed therapeutics for tuberculosis: can we harness the host?Microbiology and molecular biology reviews : MMBR · 2013Review
- Article
- Mycobacterium tuberculosis gene Rv2136c is dispensable for acid resistance and virulence in mice.Tuberculosis (Edinburgh, Scotland) · 2011Article
- Acid resistance in Mycobacterium tuberculosis.Journal of bacteriology · 2009Review
- Mycobacterial survival strategies in the phagosome: defence against host stresses.Cellular microbiology · 2009Review
- A membrane protein preserves intrabacterial pH in intraphagosomal Mycobacterium tuberculosis.Nature medicine · 2008Article
- Sustained activation of proton channels and NADPH oxidase in human eosinophils and murine granulocytes requires PKC but not cPLA2 alpha activity.The Journal of physiology · 2007Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
During the course of infection Mycobacterium tuberculosis predominantly resides within macrophages, where it encounters and is often able to resist the antibacterial mechanisms of the host. In this study, we assessed the role of macrophage phospholipases A2 (PLA2s) in defense against M. tuberculosis. Mouse bone marrow-derived macrophages (BMDMs) expressed cPLA2-IVA, cPLA2-IVB, iPLA2-VI, sPLA2-IIE, and sPLA2-XIIA. The expression of cPLA2-IVA was increased in response to M. tuberculosis, gamma interferon, or their combination, and cPLA2-IVA mediated the release of arachidonic acid, which was stimulated by M. tuberculosis in activated, but not unactivated, macrophages. We confirmed that arachidonic acid is highly mycobactericidal in a concentration- and pH-dependent manner in vitro. However, when M. tuberculosis-infected macrophages were treated with PLA2 inhibitors, intracellular survival of M. tuberculosis was not affected, even in inducible nitric oxide synthase-deficient macrophages, in which a major bactericidal mechanism is removed. Moreover, intracellular survival of M. tuberculosis was similar in cPLA2-IVA-deficient and wild-type macrophages. Our results demonstrate that the cytosolic PLA2s are not required by murine BMDMs to kill M. tuberculosis.
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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.