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Interferon‐γ signal transduction during parasite infection: modulation of MAP kinases in the infection of human monocyte cells (THP1) by Toxoplasma gondii
Author(s) -
GOMEZMARIN JORGE E.,
VALERE AUDREY,
BONHOMME ANNIE,
EL'BTAOURI HASSAN,
ANTONICELLI FRANK,
BURLET HENRIETTE,
AUBERT DOMINIQUE,
VILLENA ISABELLE,
GUENOUNOU MONCEF,
HAYE BERNARD,
PI JEAN M.
Publication year - 1998
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.1365-3024.1998.00194.x
Subject(s) - toxoplasma gondii , biology , kinase , signal transduction , microbiology and biotechnology , monocyte , cytosol , phosphorylation , mitogen activated protein kinase , extracellular , mapk14 , interferon , protein kinase a , map kinase kinase kinase , immunology , biochemistry , antibody , enzyme
We assayed mitogen‐activated protein (MAP) kinase phosphorylation in a human monocyte cell line (THP1) during their infection by Toxoplasma gondii . In addition, we tested the effect of specific MAP kinase inhibitors (PD098059 and SB203580) on parasite invasion. MAP kinase phosphorylation was increased in the cytosol and membrane fractions of THP1 infected with T. gondii . The MAP kinase phosphorylation of uninfected THP1 cells was not significantly modified by incubation for 20 h with 1000 U/ml of IFN‐γ. However, IFN‐γ treatment of infected cells significantly reduces the increase in phosphorylation caused by parasite infection. There was also MAP kinase activity in the cytosol and membrane fractions of extracellular T. gondii tachyzoites. IFN‐γ altered the distribution of activity in subcellular fractions of extracellular T. gondii tachyzoites. This indicates that IFN‐γ directly affects parasite MAP kinase activity. The results provide evidence that MAP kinase pathways participate in the infection by T. gondii and that the decrease in MAP kinase activity in infected cells caused by IFN‐γ may be involved in mediating their protective signals .