Human isolated lung preparations were passively sensitized using mouse monoclonal dinitrophenyl (DNP)-specific IgE antibodies. The contractile response to antigen (DNP-bovine serum albumin; DNP-BSA) was approximately 80% of the histamine response (50 µM: 0.20 ± 0.03 g/mm2) in bronchial muscle preparations. In passively sensitized pulmonary vascular and parenchymal preparations, the contraction to antigen was negligible. Indomethacin (1.7 µM; 30 min) did not alter the contractile response to DNP-BSA (5 µg/ml) in bronchial tissues. In passively sensitized bronchial muscle preparations stimulated with DNP-BSA, there was a significant increase (2-fold) in prostanoid production. This production was inhibited by indomethacin. These data suggest that endogenous prostaglandins may not play a role in the regulation of human isolated bronchial muscle contraction to antigen in vitro.