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Am. J. Respir. Cell Mol. Biol., Volume 27, Number 1, July, 2002 107-114

Role of MAP Kinase Activation in Interleukin-8 Production by Human BEAS-2B Bronchial Epithelial Cells Submitted to Cyclic Stretch

Séverine Oudin and Jérôme Pugin

Division of Medical Intensive Care, Departments of Internal Medicine and Genetic and Microbiology, University of Geneva, Geneva, Switzerland

Overstretching the airways during positive pressure mechanical ventilation or attacks of acute severe asthma is associated with important biologic responses. Interleukin (IL)-8-dependent neutrophil recruitment seems to play a critical role in the process of mechanical stress-induced airway inflammation. Herein, we show that human bronchial epithelial BEAS-2B cells submitted to cyclic stretch in vitro produce IL-8, at both the mRNA and protein levels. This cellular stress "turns on" activator protein (AP)-1 and cyclic AMP (cAMP)-responding elements. The mitogen-activated protein (MAP) kinases (MAPK) p44/42, SAPK/JNK, and p38 were all rapidly activated (phosphorylated) after the initiation of the cyclic strain (5-10 min). The blockade of p38 with the pharmacologic inhibitor SB203580 abrogated IL-8 production by cell stretching, and an inhibitor of the p44/42 pathway, PD98059, partially inhibited the IL-8 response. A nonspecific tyrosine kinase inhibitor, genistein, also blocked the stretch-induced IL-8 production. This suggests that MAPK, and p38 in particular, are proximal and key intracellular signaling molecules mediating cell activation in response to cyclic stretch, a mechanical strain similar to that applied to lung epithelial cells during mechanical ventilation. Pharmacologic inhibition of the p38 pathway holds promise as a new therapeutic avenue in ventilated patients.

Abbreviations: activator protein-1, AP-1; cyclic AMP, cAMP; cAMP- responding element, CRE; extracellular matrix, ECM; focal adhesion kinase, FAK; interleukin, IL; mitogen-activated protein, MAP; MAP kinase, MAPK; MAPK kinase, MAPKK; NF-kappa B, nuclear factor-kappa B; RNase protection assay, RPA; stress activated protein kinase/c-jun N-terminal kinase, SAPK/JNK; total lung capacity, TLC; ventilator-induced lung injury, VILI.




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