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ICAM-l plays an important role in inflammatory diseases. We analysed ICAM-l expression on BAL fluid cells and measured soluble ICAM-l (sICAM-I) concentrations in sent and BAL fluids from patients with extrinsic allergic alveolitis (EAA). We found significantly increased cellular ICAM-1 expression on BAL fluid lymphocytes and alveolar marcrophages, and significantly increased values of circulating and BAL fluid sICAM-l in EAA patients compared with controls. Successive measurement shows prompt decrease of both sICAM-l values in EAA patients during periods when antigen exposure was prevented. In BAL fluids from EAA patients sICAM-l values significantly correlated to neutrophil and ICAM-1+ lymphocyte counts. In EAA patients, circulating and BAL fluid sICAM-1 values has significant negative correlations to values of carbon monoxide diffusing capacity and to time intervals between last episode and sample collection. However, these values had significant positive correlation to values of alveolar arterial oxygen pressure difference. In EAA, antigen exposure appears to induce cellular ICAM-l expression on BAL fluid cells, and also appears to up-regulate shedding of ICAM-l in the alveolar lining fluid and in the circulation. The sICAM values appear to reflect disease activity of EAA. [ABSTRACT FROM AUTHOR]

ICAM-I plays an important role in inflammatory diseases. To assess level of soluble ICAM-I in the circulation and inflamed lesions, we measured levels of soluble ICAM-1 in the circulation and bronchoalvcolar lavage fluid (BALF) of patients with idiopathic pulmonary fibrosis (IPF) and with pulmonary sarcoidosis (PS) and of healthy volunteers (HV), and we also analysed ICAM-I expression of BALF cells in some patients and HV. IPF patients had significantly higher levels of circulating ICAM-I than HV, while PS patients did not. By contrast, significantly increased levels of BALF soluble ICAM-I were found in PS patients compared with those of HV, but not in IPF patients. There were no significant differences in the proportions of ICAM-1+ BALF lymphocytes in IPF patients, PS patients and HV, whereas significantly increased proportions of ICAM-I + pulmonary alveolar macrophages were found in PS patients compared with those of HV, but not in IPF patients. There was a significant positive correlation of BALF soluble ICAM-I levels to BALF lymphocyte proportions in PS patients. Although the source of BALF soluble ICAM-l is unclear, BALF soluble ICAM-1 appears to reflect the grade of local activity of sarcoidosis. An interesting discrepancy between soluble ICAM-1 levels in the circulation and BALF was found in IPF patients, and this might be an important clue to an understanding of this disorder. [ABSTRACT FROM AUTHOR]