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Mechanisms of apoptosis in murine fibroblasts by two intracellular protozoan parasites, Toxoplasma gondii and Neospora caninum
Author(s) -
Nishikawa Yoshifumi,
Makala Levi,
Otsuka Haruki,
Mikami Takeshi,
Nagasawa Hideyuki
Publication year - 2002
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1046/j.1365-3024.2002.00476.x
Subject(s) - neospora caninum , toxoplasma gondii , biology , apoptosis , dna fragmentation , fas ligand , intracellular parasite , monoclonal antibody , interferon gamma , neospora , tunel assay , programmed cell death , virology , antibody , immunology , immune system , biochemistry
Summary Studies to clarify the mechanisms of apoptosis in host cells, A31 (BALB/3T3 clone A31 fibroblasts), caused by two intracellular protozoan parasites, Toxoplasma gondii and Neospora caninum , were carried out in an in vitro system. The viability of N. caninum‐ infected cells was significantly reduced following treatment with mouse interferon (IFN)‐γ. By contrast, mouse IFN‐γ treatment had no significant effect on the induction of apoptosis in T. gondii ‐infected cells. Apoptosis of N. caninum ‐infected and mouse IFN‐γ‐treated cells was shown to be associated with increased DNA fragmentation, and increased caspase‐3 and ‐8 activity, and the administration of caspase‐3 and ‐8 inhibitors inhibited cell death. FasL expression was clearly induced by N. caninum ‐infection and IFN‐γ treatment compared to the T. gondii‐ infected cells and the uninfected control with or without IFN‐γ treatment. The reduction in host‐cell viability was prevented with the addition of antimouse FasL monoclonal antibody (mAb). Moreover, TUNEL analyses indicated that apoptosis was induced by the treatment with Fas mAb in both T. gondii and N. caninum ‐infected cells. These results suggest that the Fas/FasL pathway may play a crucial role in the induction of apoptosis in N. caninum ‐ and T. gondii ‐infected cells mediated by IFN‐γ.