Title
Role of oxidative stress and apoptosis in the cellular response of murine macrophages upon **Leishmania** infectionRole of oxidative stress and apoptosis in the cellular response of murine macrophages upon **Leishmania** infection
Author
Faculty/Department
Faculty of Pharmaceutical, Biomedical and Veterinary Sciences. Pharmacy
Faculty of Medicine and Health Sciences
Research group
Translational Pathophysiological Research (TPR)
Laboratory for Microbiology, Parasitology and Hygiene (LMPH)
Publication type
article
Publication
London,
Subject
Biology
Human medicine
Source (journal)
Parasitology. - London, 1908, currens
Volume/pages
139(2012):11, p. 1429-1437
ISSN
0031-1820
1469-8161
ISI
000309739800003
Carrier
E
Target language
English (eng)
Full text (Publishers DOI)
Affiliation
University of Antwerp
Abstract
Leishmania parasites are able to survive in the macrophage, one of the most hostile environments of the vertebrate host. The present study investigated how Leishmania infection influences these host cell defence mechanisms. Macrophages were infected with antimony-susceptible and -resistant Leishmania strains. Free radical production in Leishmania-infected macrophages was measured by electron paramagnetic resonance. Apoptosis was detected with fluorescence microscopy using Annexin-V FITC labelling and with Western blotting to detect caspase-3 cleavage. Independent of their drug susceptibility profile or species background, all studied Leishmania strains induced a similar increase in free radical production in macrophages. O2 ●− production was significantly elevated during phagocytosis of the stationary phase promastigotes. Conversely, NO levels increased later in the infection and none of the strains induced capsase-3 cleavage. Leishmania donovani infection led to phosphatidylserine externalization only in RAW 264.7 cells. After an initial burst of O2 ●− during phagocytosis of promastigotes, amastigotes protect themselves by decreasing the O2 ●− production to the basal level. An increased NO production was observed 6 h after infection. Finally, induction of cell death is probably not essential in the survival of the parasite within the macrophage.
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