In the present study, using a commercial monoclonal antibody against CD18 developed for immunostaining but shown to block CD18 function [10], [44], [45], we confirmed our previous finding that septic pulmonary microvascular albumin leak is mediated through CD18-dependent interaction, and further illustrated the importance of PMN-MVEC physical interaction in initiating endothelial dysfunction. This evidence concerns the gene ITGB2 and endothelial dysfunction.