Journal of Occupational Health
Online ISSN : 1348-9585
Print ISSN : 1341-9145
ISSN-L : 1341-9145
Cytokine Production by Splenocytes and Thymocytes in Mice after Intranasal Exposure to Toluene Diisocyanate
Kul-Cheng ZHENGMakoto ARIIZUMIHidemi TODORIKIMasaki SHINJO
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1998 Volume 40 Issue 4 Pages 279-284

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Abstract
Cytokine Production by Splenocytes and Thymocytes in Mice after Intranasal Exposure to Toluene Diisocyanate: Kui-Cheng ZHENG, et al. Department of Preventive Medicine, School of Medicine, University of the Ryukyus—To determine the status and the role of cytokines in occupational asthma induced by toluene diisocyanate (TDI), we performed a quantitative analysis of cytokine profiles by means of splenocytes and thymocytes from an asthmatic murine model induced by TDI. Female BALB/c mice were treated with two courses of intranasal application of 5% TDI in ethyl acetate for 5 consecutive days each time separated by a one week rest. The control group of mice were similarly treated with vehicle. A week after the second sensitization, both groups of mice were provoked by applying 2.5% of TDI in vehicle, and nasal responses were scored for ten minutes. The results show that the TDI-sensitized group of mice exhibited the nasal allergic-like responses of sneezing and hyperrhinorrhea. Interleukin (IL)-4, IL-5 production by splenocytes, thymocytes and the total serum IgE level in TDI-sensitized mice were significantly higher than that in control mice. IL-2 production by splenocytes and IL-2, IFN-γ by thymocytes in both control and TDI-sensitized groups were not significantly different. IFN-γ produced by splenocytes was significantly higher in TDI-sensitized mice than that in control mice. In TDI-sensitized mice, the total serum IgE level was significantly positively correlated with IL-4 and IL-5 production by splenocytes and thymocytes, respectively. These findings suggest that splenocytes and thymocytes preferentially secrete Th2 type cytokines during murine asthma and these cytokines may play an important role in the pathogenesis of TDI-induced occupational allergic asthma.
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