Abstract 63 Allergy and Immunology Platform, Monday, 5/3

There is increasing evidence suggesting that lung surfactant proteins. A (SP-A) and D (SP-D) play a protective role in the complicated pulmonary defense against pathogens. In this study, the roles of these surfactant proteins in allergic bronchial inflammation were evaluated in a mite allergen (Dermatophagoides pteronyssinus, Der p)-sensitized murine model of asthma. The results showed that there were markedly reduced SP-A and SP-D levels in the bronchoalveolar lavage fluid (BALF) from Der p- sensitized BALB/c mice at 48 to 72 hr after allergen challenge (AC). The decrease in surfactant protein levels after AC was found to correlate over the same time period with an impairment of surface activity of BALF as detected by the pulsating bubble method. In a cell proliferation assay, both SP-A and SP-D were able to reduce, in a dose-dependent manner, the incorporation of [3H]-thymidine into Der p-stimulated intrapulmonary lymphocytes proliferation. Moreover, this inhibitory effect of surfactant proteins was observed in naive mice challenged with saline or allergen, and also in sensitized mice challenged with saline, while only a mild degree (< 9 %) of suppression on already activated lymphocytes was seen in sensitized mice after AC. To evaluate the effect of exogenous surfactant on allergen-induced bronchial inflammation, Survanta and/or a recombinant fragment of SP-D was given to sensitized mice before or after AC. Survanta had a preventive effect on allergic inflammation when administrated 1 hr before AC, while it had only slight effect on total cell numbers and cellular distributions in BALF when given after AC. Intratracheal instillation of recombinant fragment of SP-D reduced total cell numbers and decreased eosinophil infiltration in BAL at 6 hr after AC, but had no effect on bronchial inflammation when administrated before AC. These results provide further in vivo evidences that surfactant proteins may be involved in allergic bronchial inflammation and in the pathogenesis of asthma.

This work was supported by grants NSC 88-2314-B-006-120 and NSC 88-2314-B006-11-M50 from National Science Council, Taiwan.