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Leishmania major ‐mediated prevention of programmed cell death induction in infected macrophages is associated with the repression of mitochondrial release of cytochrome c
Author(s) -
Akarid Khadija,
Arnoult Damien,
MicicPolianski Juliette,
Sif Jamila,
Estaquier Jérôme,
Ameisen Jean Claude
Publication year - 2004
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1001877
Subject(s) - biology , leishmania , intracellular parasite , macrophage , secretion , programmed cell death , effector , psychological repression , microbiology and biotechnology , mitochondrion , leishmania major , cytokine , cytochrome c , intracellular , immunology , apoptosis , in vitro , gene expression , parasite hosting , gene , genetics , biochemistry , world wide web , computer science
Leishmania are obligate, intracellular parasites of macrophages in their vertebrate hosts, including humans, in which they cause disease. Here, we report that in vitro infection with Leishmania major protects murine bone marrow‐derived macrophages against programmed cell death (PCD) induced by deprival of macrophage‐colony stimulating factor and delays PCD caused by treatment with staurosporine, a broad inducer of PCD. This preventive effect was observed in macrophages from L. major ‐susceptible BALB/c and L. major ‐resistant C57BL/6 mice, indicating that repression of PCD did not depend on genetic background‐specific regulation of T helper cell type 1 (Th1)/Th2 cytokine secretion. Prevention of effector caspase activation and PCD was associated with a repression of mitochondrial release of cytochrome c and did not involve the nuclear factor‐κB pathway. The capacity of L. major to delay PCD induction in the infected macrophages may have implications for Leishmania pathogenesis by favoring the invasion of its host and the persistence of the parasite in the infected cells.