ArticleThe Journal of biological chemistry2014
Leishmania donovani prevents oxidative burst-mediated apoptosis of host macrophages through selective induction of suppressors of cytokine signaling (SOCS) proteins.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 62 citations in OpenAlex.
- Article
- Oxidative Stress and Survival ofExpert reviews in molecular medicine · 2025Review
- The developing role of NRF2 and HMOX1 in treatment response of cutaneous leishmaniasis.Scientific reports · 2025Article
- An inclusive assessment of apoptosis mechanisms inCurrent research in parasitology & vector-borne diseases · 2025Review
- Mechanisms regulating host cell death duringmBio · 2024Review
- The pathogenicity and virulence of Leishmania - interplay of virulence factors with host defenses.Virulence · 2022Review
- Transcriptional profiling of macrophages reveals distinct parasite stage-driven signatures during early infection by Leishmania donovani.Scientific reports · 2022Article
- Immune Responses in Leishmaniasis: An Overview.Tropical medicine and infectious disease · 2022Review
- Intranasal vaccine from whole Leishmania donovani antigens provides protection and induces specific immune response against visceral leishmaniasis.PLoS neglected tropical diseases · 2021Article
- Management of cell death in parasitic infections.Seminars in immunopathology · 2021Review
- Transcription Factors Interplay Orchestrates the Immune-Metabolic Response ofFrontiers in cellular and infection microbiology · 2021Review
- Functional aspects, phenotypic heterogeneity, and tissue immune response of macrophages in infectious diseases.Infection and drug resistance · 2019Article
- The Paradoxical Leishmanicidal Effects of Superoxide Dismutase (SOD)-Mimetic Tempol inFrontiers in cellular and infection microbiology · 2019Article
- In vitro activity of Morinda citrifolia Linn. fruit juice against the axenic amastigote form of Leishmania amazonensis and its hydrogen peroxide induction capacity in BALB/c peritoneal macrophages.BMC research notes · 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
- Ammonium trichloro [1,2-ethanediolato-O,O']-tellurate cures experimental visceral leishmaniasis by redox modulation of Leishmania donovani trypanothione reductase and inhibiting host integrin linked PI3K/Akt pathway.Cellular and molecular life sciences : CMLS · 2018Article
- Leptin Functions in Infectious Diseases.Frontiers in immunology · 2018Review
- Hypoxia, Hypoxia-Inducible Factor-1α, and Innate Antileishmanial Immune Responses.Frontiers in immunology · 2018Review
- The role of PD-1 in regulation of macrophage apoptosis and its subversion byClinical & translational immunology · 2017Article
- Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the mechanisms for establishment of infection employed by intra-macrophage pathogen-like Leishmania is inhibition of oxidative burst-mediated macrophage apoptosis to protect their niche for survival and replication. We tried to elucidate the underlying mechanism for this by using H2O2 for induction of apoptosis. Leishmania donovani-infected macrophages were much more resistant to H2O2-mediated apoptosis compared with control. Although infected cells were capable of comparable reactive oxygen species production, there was less activation of the downstream cascade consisting of caspase-3 and -7 and cleaved poly(ADP)-ribose polymerase. Suppressors of cytokine signaling (SOCS) 1 and 3 proteins and reactive oxygen species scavenging enzyme thioredoxin, known to be involved in stabilization of protein-tyrosine phosphatases, were found to be induced during infection. Induction of SOCS proteins may be mediated by Egr1, and silencing of Socs1 and -3 either alone or in combination resulted in reduced thioredoxin levels, enhanced activation of caspases, and increased apoptosis of infected macrophages. The induction of protein-tyrosine phosphatases, thioredoxin, SOCS, and Egr1 in L. donovani-infected macrophages was found to be unaffected by H2O2 treatment. SOCS knocked down cells also displayed decreased parasite survival thus marking reduction in disease progression. Taken together, these results suggest that L. donovani may exploit SOCS for subverting macrophage apoptotic machinery toward establishing its replicative niche inside the host.
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