Immunological challenge of human lung parenchyma causes formation of arachidonate metabolites: prostaglandin D2 (PGD2) (70% of the formed mediators), leukotrienes E4 (LTE4) (15%) and D4 (LTD4) (10%). Leukotriene B4 (LTB4) was barely detectable (2%). Inhibition of PGD2 formation by indomethacin (15 microM) was approximately 90%, but was not accompanied by redistribution of arachidonate metabolism towards sulphidopeptide leukotrienes, as postulated for aspirin-sensitive asthma. Specific binding sites for leukotrienes C4 (LTC4) have been identified in membrane preparations of human bronchi. Binding of 3H-LTC4 is rapid (1 min) and quickly reversible following addition of excess. The sites are specific for LTC4 and competition curves fitted a two-site model. Moreover, clinical studies on specific endobronchial challenge of patients allergic to Dermatophagoides pteronyssinus, revealed narrowing of bronchial diameter and oedema of the bronchial mucosa; these symptoms were accompanied by an increase of immunoreactive-LTC4 and PGD2 present in the bronchial lavage fluids.