Role of mast cells in antigen-induced airway inflammation and bronchial hyperresponsiveness in rats

The participation of mast cells in the induction of antigen-induced airway inflammation and bronchial hyperresponsiveness (BHR) to acetylcholine (ACh) was investigated using pharmacological agents and mast cell-deficient rats (Ws/Ws). A significant increase in the number of leukocytes in bronchoalve olar lavage fluid (BALF) and bronchial responsiveness to ACh were observed 24 h after antigen (ovalbumin) challenge in sensitized Brown-Norway (BN) ra ts. Disodium cromoglycate and terfenadine did not inhibit antigen-induced a irway inflammation and BHR in sensitized BN rats. In contrast, cyclosporin A (CyA), FK-506 and prednisolone significantly inhibited antigen-induced ai rway inflammation and BHR in sensitized BN rats. In addition, disodium crom oglycate, terfenadine and prednisolone, but not CyA and FK-506, inhibited h omologous passive cutaneous anaphylaxis in rats. Furthermore, a significant increase in the number of leukocytes in BALF and BHR was also observed in Ws/Ws rats 24 h after inhalation of antigen; however, the magnitude of BHR in Ws/Ws rats was lower than that in the congenic rats. These findings sugg est that mast cells play a partial role in the development of antigen-induc ed BKR in rats and that the induction of BHR is barely suppressed by mast c ell stabilizing agents.