Our previous work in a murine sepsis model identified that pulmonary microvascular/PMVEC barrier dysfunction, as reflected by enhanced albumin leak and oxidant stress required the presence of both alveolar macrophages and PMN, CD18-dependent PMN-PMVEC adhesion, increased nitric oxide (NO) production from inducible NO synthase (iNOS), and iNOS/NADPH oxidase-dependent peroxynitrite-mediated signaling [17–19, 34–36]. This evidence concerns the gene ALB and Sepsis.