In septic ALI, pulmonary microvascular dysfunction is the result of direct interaction of MVEC with activated PMNs, as well as the action of multiple inflammatory mediators (e.g. LPS, cytokines, and increased nitric oxide (NO) production following enhanced expression of inducible NO synthase) [10], [11], [13], [25]–[37]. This evidence concerns the gene NOS2 and acute respiratory distress syndrome.