Ventilation-induced neutrophil infiltration depends on c-Jun N-terminal kinase.

摘要: Positive pressure ventilation with large VTs has been shown to cause release of cytokines, including macrophage inflammatory protein-2 (MIP-2), a functional equivalent human interleukin-8. The mechanisms regulating ventilation-induced cytokine production are unclear. Based on our previous in vitro model lung cell stretch, we hypothesized that high VT MIP-2 is dependent the activation c-Jun N-terminal kinase (JNK). We exposed C57BL/6 mice (30 ml/kg) or low (6 mechanical for 5 hours. High neutrophil migration into lung, protein production, messenger RNA expression, and JNK activation. Large knockout pharmacologic inhibition SP600125 attenuated sequestration blocked expression production. conclude stretch vivo results increased which was, at least part, upon pathway.