Naoki Kawada, Hiroyuki Tanaka, Toshiaki Takizawa, Takatoshi Yamada, Yoshimasa
Takahashi, Taisei Masuda, Naoki Inagaki and Hiroichi Nagai*
Department of Pharmacology, Gifu Pharmaceutical University, 5-6-1 Mitahora-higashi,
Gifu 502-8585, Japan
*Corresponding author. FAX: +81-58-237-8584
E-mail: nagai@gifu-pu.ac.jp
Abstract: 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 bronchoalveolar
lavage fluid (BALF) and bronchial responsiveness to ACh were observed 24
h after antigen (ovalbumin) challenge in sensitized Brown-Norway (BN) rats.
Disodium cromoglycate and terfenadine did not inhibit antigen-induced airway
inflammation and BHR in sensitized BN rats. In contrast, cyclosporin A (CyA),
FK-506 and prednisolone significantly inhibited antigen-induced airway inflammation
and BHR in sensitized BN rats. In addition, disodium cromoglycate, terfenadine
and prednisolone, but not CyA and FK-506, inhibited homologous 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 suggest that mast cells play a partial
role in the development of antigen-induced BHR in rats and that the induction
of BHR is barely suppressed by mast cell stabilizing agents.
Keywords: Airway inflammation, Bronchial hyperresponsiveness, Brown-Norway
rat, Mast cell, Ws/Ws rat
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