ANTI-INTERCELLULAR ADHESION MOLECULE-1 ANTIBODY AND INTERCELLULAR-ADHESION MOLECULE-1 GENE DEFICIENCY DO NOT PREVENT PULMONARY NEUTROPHIL RECRUITMENT IN POLYMICROBIAL SEPSIS

The intercellular adhesion molecule (ICAM)-1 is expressed constitutive ly in normal lungs and increased in pulmonary inflammation. Whether in creased ICAM-1 expression in the lung contributes to neutrophil seques tration during lung inflammation in sepsis is unclear. We tested this hypothesis in mice after systemic sepsis from cecal ligation and punct ure (CLP). ICAM-1 expression in mouse CLP lung tissue was found to inc rease with time. The time course of lung ICAM-1 up-regulation correlat ed with increases in lung myeloperoxidase (MPO) activity and neutrophi l sequestration by light microscopy. The monoclonal IgG2b rat anti-mou se antibody, an anti-ICAM-1 antibody (YN1/1.7), administered intraveno usly at doses of 3, 10, or 30 mg/kg, however, did not decrease the lun g MPO levels compared with nonimmune rat IgG. In support of these find ings, lung MPO content in ICAM-1-deficient mice that underwent CLP was significantly higher than similarly treated ICAM-1-sufficient mice. O ur results suggest that neutrophil sequestration in the mouse lung aft er CLP is not dependent on ICAM-1.