Management of artificial respiration worsens acute lung injury.-Investigation and influence of mechanism by molecular biological approach-

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Alveolar epithelial cells type II (AEC-II) are thought to play an important role in the pathogenesis of acute lung injury because AEC-II can produce many types of pro-inflammatory cytokines and chemokines. Especially, Interleukin-8 (IL-8) plays an important role in this inflammatory response. AEC-II are exposeed to mechanical stretch during breathing and mechanical ventilation. Increased stretch may contribute to lung injury. The purpose of this study is to elucidate the effects of cell stretch on endotoxin-induced interleukin-8 (IL-8) production from cultured rat AEC-II.After isolation of rat AEC-II, cells were cultured for 48h. LPS (lipopolysaccaraide) increased rat GRO/CINC (IL-8) measured by ELISA in rat alveolar type II cell cultured media. Cells were stretched using mechanical stretch machine (Flexcell). At 3h, 6h, 12h and 24h, the cell media were collected and GRO/CINC (IL-8) were measured by ELISA. The concentration of GRO/CINC (IL-8) increased time-dependently in 24h. LPS & cell Stretch induced additional increase compared with each study.These results showed cell damage induced by cell stretch was similar to ventilator-induced lung injury and LPS & stretch means mechanical ventilation in septic state in clinical. This model may help for future therapy and mechanizm for acute lung injury induced by sepsis.