Thus, our findings that nmMLCK controls ICAM-1 expression in EC in vitro and in the lung in vivo and that the blockade of ICAM-1 causes a marked reduction in thrombin-induced lung PMN sequestration in mice underscores the importance of endothelial nmMLCK/ICAM-1 axis in the mechanism of lung vascular inflammation. This evidence concerns the gene ICAM1 and inflammation.