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A helper T(Th)1-mediated response is known to enhance cell-mediated immunity, while a Th2-mediatedresponse is associated with the humoral immunity that is elevated IgE levels and eosinophilia. Prostaglandin(PG)E2 results in the decreased capability of lymphocytes to produce Th1 cytokines, with a shift toward a Th2cytokine response. Chlorpyrifos (CPF) has been reported to impair the blastogenesis and response of Tlymphocytes. CPF also induces delayed febrile effects, which results from the activation of COX-PGE2pathway. The purpose of this study is to determine the effect of CPF on the in vitroproduction of Th cytokinesand the role of PGE2 on the CPF-induced production of Th cytokines. Splenocytes obtained from maleBALB/c mice were pretreated with CPF(0.1, 1, 10 and 100M) in the presence or absence of indomethacin orPGE2 for 12 h and then were incubated with concanavalin (Con) A for 48 h. These results showed that CPFremarkedly reduced the production of splenic interleukin (IL)-2 and interferon (IFN)-γin a dose-dependentmanner. CPF significantly increased the splenic IL-4 production at low doses(0.1 and 1M) but did not affectat high doses(10 and 100M). Indomethacin reduced the CPF-decreased production of IL-2 and IFN-γin adose-dependent manner and significantly attenuated the production of IL-4 increased by CPF 0.1M. Highdose of CPF significantly reduced the PGE2-decreased production of IL-2 and IFN-γ, while the PGE2-induced production of IL-4 was significantly enhanced by CPF 1M. These findings suggest that CPF maydown-regulate the immune response of Th1 type by the suppressed production of IL-2 and IFN-γ, with ashift toward a Th2 cytokine response. The CPF-decreased production of Th1 cytokines may not be mediatedby endogenous PGE2. Also, CPF may attenuate the exogenous PGE2-decreased Th1 immune response in adose-dependent manner but may affect dose-independently the PGE2-induced Th2 immune response.