The pathogenesis of ALI remains unclear, largely a consequence of the heterogeneity of patients coming into the ICU and the broad clinical features characteristic of ALI [1, 19] . The cellular mechanisms contributing to lung tissue injury in ALI are for the most part unknown, [20] although the potential involvement of neutrophils in the development of ALI remains the focus of many studies (see for example [21, 22] ). In particular, neutrophil-derived products (e.g., extracellular matrix degrading proteinases and reactive oxygen species), inflammatory fibrotic cytokines, and growth factors [23] [24] [25] [26] have been postulated as causative agents underlying the onset and progression of disease [27] .