Leukocyteendothelial adhesion molecules are involved in the initial state of the recruit ment and migration of inflammatory leukocytes from the circulation to sites of inflammation. In allergic inflammation, administ-ration of anti-ICAM-1 monoclonal antibodies into monkeys resulted both in reduced eosinophil infiltration into the lung and in reduced airway hyperresponsiveness, and upregulation of ICAM-1 expression was observed on the endothelium, the bronchial epithelium, and eosinophils, suggesting an important role for ICAM-1 in the pathogenesis of bronchial asthma. To our knowledge, there has been few previous reports concerning solublelCAM-1 (sICAM-l) in patients with atopic bronchial asthma after allergen challenge. If the levels of sICAM-1 vary between bronchial asthma patients and normal controls, this variance would be very useful to assess the state of this disease. Therefore, we attempted to measure the levels of sICAM-1 from 17patients with atopic bronchial asthma. sICAM-1 levels in sera from patients with bronchial asthma were measured at 8 hour after allergen challenge with house dust mite, and prechallenge periods. sICAM-1 levels in BAL fluids were also measured at 30min and 8hour after allergen challenge. sICAM-1 levels in sera from bronchial asthma in prechallenge conditions were higher than in normal control subjects, and sICAM-1 levels in sera from bronchial asthma patients in 8hour after allergen challenge were higher than those in sera obtained during prechallenge periods. sICAM- 1 levels in BAL fluids from bronchial asthma patients in 8hour after allergen challenge were significantly higher than in 30min after allergen challenge. These results suggest that higher levels of sICAM-1 in sera and BAL fluids reflect the upregulation of ICAM-1 expression in allergic bronchial asthma and it may take a role in the pathogenesis of atopic bronchial asthma.