Abstract
This study was aimed at investigating the cytokine status and their gene expressions in airways of asthmatic mouse caused by toluene diisocyanate (TDI). After the mice were exposed to TDI vapor for 5 consecutive days, bronchoalveolar lavage (BAL) was carried out and the cells in the BAL fluid were counted. Lung histological test was conducted to analyse the inflammatory status in the airways. Total serum IgE and IL-4 and IL-5 concentrations in the BAL fluid were determined with ELISA kits. RT-PCR was applied to investigate IL-4 and IL-5 mRNA from BAL cells. The airway cell count and histological analysis showed that TDI exposure resulted in airway inflammatory responses characterized by marked infiltration of eosinophils in the central and peripheral airways. Total serum IgE was significantly increased in the TDI-exposed mice. IL-4 and IL-5 productions in the BAL fluid were significantly enhanced in the mice exposed to TDI, but in BAL cells IL-4 and IL-5 mRNA were slightly enhanced without any significant difference compared to the control mice. These results further support the hypothesis that Th2 cytokines are predominantly produced in TDI-induced airway hypersensitivity, but our data were not able to indicate the exact source of these cytokines and we could not determine whether the change in cytokines in the airways was controlled by the gene transcription level.
