“…We must consider the possibility that obesity may alter ARDS pathogenesis by "priming" the lung for inflammatory insult and amplifying the early inflammatory response (thus lowering the threshold to initiate ARDS), while at the same time accelerating a subsequent transition to the recovery phase. How obesity may change the "inflammatory twitch" of the lung (35) is only beginning to be understood, but on the basis of recent mouse modeling, this appears to include both baseline pulmonary vascular "priming" (34) and neutrophil functional impairment (28,36,37), as well as other effects of elements of the metabolic syndrome, including hyperglycemia (29,36), dyslipidemia (28,36,37), hypoadiponectinemia (34,38), and hyperleptinemia (39). For example, recent studies by Shah and colleagues (34), examining several mouse strains that vary in their susceptibility to diabetes in a dietinduced obesity (DIO) model, have highlighted the complex interplay between glucose intolerance and lung injury.…”