

Author: Nario Ricardo C Hubbard Andrea K
Publisher: Taylor & Francis Ltd
ISSN: 1087-2620
Source: Journal of Toxicology and Environmental Health, Vol.49, Iss.6, 1996-12, pp. : 599-618
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Abstract
Although the pathogenic mechanisms underlying silica induced lung damage are well described few studies have examined the expression and role of adhesion molecules in lung injury induced by this particle Here we report that intratracheal instillation of silica crystals quartz SI into the lungs of C57Bl 6 mice results in a significant increase 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 24 h cell influx and lung injury rather than in the initiation of these events 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 significantly decreased the influx of neutrophils PMNs into the alveoli and the levels of lung tissue ICAM 1 and yet had no effect on measures of lung injury or increased collagen deposition These data suggest that increased ICAM 1 expression in lung tissue following exposure to silica plays a partial role in the trafficking of neutrophils into the airways
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