The occurrence of late asthmatic response (LAR) is effectively prevented by corticosteroids, but not all by beta-adrenergic drugs. LAR is considered to be of great clinical and therapeutic importance and to be involved in the progression of bronchial asthma into a severe or even an intractable form. However the exact mechanism of the occurrence of LAR remains obscure in many respects. LAR is believed to be due to type I allergy. In guinea pigs, a positive bronchial inhalation challenge following passive sensitization with allogeneic antibody does not induce LAR or eosinophilic infiltration of lung tissue. This experimental fact led us to surmise that LAR would seem likely to be elicited in passively sensitized animals if pronounced eosinophilic infiltration can be induced concurrently and to conduct an experiment with conjoined inhalation of platelet activating factor (PAF). PAF, which has a chemotactic activity for eosinophils, was administered to passively sensitized animals in attempt to examine a role of eosinophils in LAR. A goodly number of animals developed LAR on additional PAF inhalation. These animals, when compared with those without LAR, showed a significantly larger proportion of eosinophils in BALF (p less than 0.05) with an upward tendency for the proportion of neutrophils. Histologically, there was noted a striking association between LAR and eosinophilic infiltration of the bronchial submucosa. These results suggest that anti-IgE antibody is deeply involved in the elicitation of LAR, stressing the importance of eosinophilic infiltration.