ArticleMedical microbiology and immunology2013
Infection of neutrophil granulocytes with Leishmania major activates ERK 1/2 and modulates multiple apoptotic pathways to inhibit apoptosis.
Article in Medical microbiology and immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
- Article
- Apoptosis as an evolutionary battleground: pathogen pressure and the shaping of programmed cell death pathways.Frontiers in cell and developmental biology · 2026Review
- Transcriptome profiling of L. infantum-infected human macrophages reveals sex-specific type I interferon induction.PLoS pathogens · 2025Article
- An inclusive assessment of apoptosis mechanisms inCurrent research in parasitology & vector-borne diseases · 2025Review
- Mechanisms regulating host cell death duringmBio · 2024Review
- Apoptosis and its pathways as targets for intracellular pathogens to persist in cells.Parasitology research · 2023Review
- Neutrophil Survival Signaling DuringFrontiers in cellular and infection microbiology · 2022Article
- Management of cell death in parasitic infections.Seminars in immunopathology · 2021Review
- The Paradox of a Phagosomal Lifestyle: How Innate Host Cell-Frontiers in immunology · 2021Review
- Role of Host and Parasite MIF Cytokines duringTropical medicine and infectious disease · 2020Review
- Cinnamomum cassia exhibits antileishmanial activity against Leishmania donovani infection in vitro and in vivo.PLoS neglected tropical diseases · 2019Article
- Malaria, anemia, and invasive bacterial disease: A neutrophil problem?Journal of leukocyte biology · 2019Review
- Infection of Human Neutrophils WithFrontiers in cellular and infection microbiology · 2019Article
- Article
- Caffeic acid combined with autoclaved Leishmania major boosted the protection of infected BALB/c mice by enhancing IgG2 production, IFN-γ/TGF-β and iNO synthase/arginase1 ratios, and the death of infected phagocytes.Inflammopharmacology · 2018Article
- Role of glutathione, ROS, and Bcl-xL in the inhibition of apoptosis of monocyte-derived dendritic cells by Leishmania mexicana promastigotes.Parasitology research · 2018Article
- Review
- Survival Mechanisms Used by SomeFrontiers in immunology · 2017Review
- Influence of Microbes on Neutrophil Life and Death.Frontiers in cellular and infection microbiology · 2017Review
- Enhanced survival of Leishmania major in neutrophil granulocytes in the presence of apoptotic cells.PloS one · 2017Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophil granulocytes provide the first line of defense against bacterial, fungal, and parasitic infections. They phagocytose and kill many invading pathogens. Certain pathogenic microorganisms such as the intracellular protozoan parasite Leishmania major (L. major) can survive inside neutrophils. Mature neutrophils have a very short life span due to spontaneous apoptosis. Previously, we have reported that infections with L. major are able to delay spontaneous apoptosis. In the present study, we addressed the underlying mechanisms of regulation of both extrinsic and intrinsic apoptosis. We show that interaction with L. major transiently activates ERK1/2 phosphorylation. Pharmacological inhibition of ERK1/2 phosphorylation reversed the apoptosis delay. Moreover, infection leads to the enhanced and sustainable expression of the anti-apoptotic proteins Bcl-2 and Bfl-1, respectively. As downstream events, the release of cytochrome c from mitochondria and processing of caspase-6 were inhibited. We also confirm that infection with L. major results in reduced FAS expression on the surface of neutrophils. The presented data indicate that infection with L. major affects both intrinsic as well as extrinsic pathways of neutrophil apoptosis. Enhanced life span of host neutrophils enables the parasite to survive within neutrophils.
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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.