SILICA EXPOSURE INCREASES EXPRESSION OF PULMONARY INTERCELLULAR-ADHESION MOLECULE-1 (ICAM-1) IN C57BL 6 MICE/

Although the pathogenic mechanisms underlying silica-induced lung dama ge are well described, few studies have examined the expression and ro le of adhesion molecules in lung injury induced by this particle. Here we report that intratracheal instillation of silica crystals (alpha q uartz) (SI) into the lungs of C57BI/6 mice results in a significant in crease in levels of intercellular adhesion molecule-1 (ICAM-1) in lung tissue and in lung lavage fluid. This increased expression of ICAM-1 appeared to be associated with later (greater than or equal to 24 h) c ell influx and lung injury rather than in the initiation of these even ts. Exposure of mice to the nontoxic particle titanium dioxide did not elicit increased expression of ICAM-1 in lung tissue or lavage fluid. Passive administration of rat anti-mouse ICAM-1 monoclonal antibody s ignificantly decreased the influx of neutrophils (PMNs) into the alveo li and the levels of lung tissue ICAM-1 and yet had no effect on measu res of lung injury or increased collagen deposition. These data sugges t that increased ICAM-1 expression in lung tissue following exposure t o silica plays a partial role in the trafficking of neutrophils into t he airways.