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In this study, we report on the role of epidermal growth factor receptor (EGFR) transactivation in H. pylori lipopolysaccharide (LPS)-elicited induction in gastric mucosal expression of COX-2 and iNOS. Materials and methods We aimed to demonstrate that the LPS-induced p38 activation along with MMPs are of critical significance to EGFR transactivation that leads to up-regulation in the activation of ERK signalling cascade, amplification in iNOS and COX-2 induction, and consequently to the excessive increase in gastric mucosal PGE2 and NO generation. Results EGFR transactivation results in the amplification of the LPS-induced ERK phosphorylation and up-regulation in ERK-mediated IKK-β activation for the enhanced induction of NFκB-dependent expression of iNOS. The rise in iNOS-dependent NO generation, in turn, leads to an up-regulation in COX-2 activation through Snitrosylation and excessive PGE2 production. Conclusion Taken together, our data provide strong indications of the involvement of EGFR transactivation in the amplification of ERK signalling cascade associated with up-regulation in gastric mucosal induction of iNOS and COX-2, and excessive NO and PGE2 generation in response to H. pylor

oa inflammation

Role of epidermal growth factor receptor transactivation in the amplification of Helicobacter pylori-elicited induction in gastric mucosal expression of cyclooxygenase-2 and inducible nitric oxide synthase