INTERCELLULAR-ADHESION MOLECULE-1 MEDIATES ACID ASPIRATION-INDUCED LUNG INJURY

Acid-aspiration-induced injury is one of the leading causes of adult r espiratory distress syndrome. Intercellular adhesion molecule-1 (ICAM- 1) is a ligand for lymphocyte-function-associated antigen-1 alpha (LFA -1 alpha), and it has been shown to be required for leukocyte migratio n into inflamed areas. The purpose of this report was to investigate t he role of the ICAM-1/LFA-1 alpha pathway in a rat model of acid-aspir ation-induced injury. Animals received 3.0 ml/kg HCl (0.1 N; pH, 1.0) intratracheally pretreated with control monoclonal antibodies (mAbs) ( HCl group) or anti-ICAM-1 and LFA-1 alpha mAbs (Test group). In the HC l group, increases in lung resistance (RL) (229 +/- 23% baseline), lun g wet-to-dry weight ratio (W/D) (11.9 +/- 0.4), protein concentration (TP) (0.447 +/- 0.054 mg/ml), and the number of neutrophils (PMN) (159 .0 +/- 19.4 x 10(4)) Of bronchoalveolar lavage fluid were observed. In the Test group, HCl-induced injury was significantly reduced (RL, 122 +/- 7% baseline; W/D, 7.2 +/- 0.1; TP, 0.277 +/- 0.016 mg/ml; PMN, 8. 8 +/- 0.8 x 10(4)). The administration of mAbs to ICAM-1 and LFA-1 alp ha after HCl instillation partially attenuated HCl-induced responses. These observations suggest that the ICAM-1/LFA-1 alpha pathway might b e involved in the pathogenesis of adult respiratory distress syndrome caused by acid aspiration.