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Mediators of Inflammation
Volume 2014, Article ID 128919, 12 pages
http://dx.doi.org/10.1155/2014/128919
Research Article

Anti-Inflammatory Mechanism of Polyunsaturated Fatty Acids in Helicobacter pylori-Infected Gastric Epithelial Cells

1Department of Food and Nutrition, Brain Korea 21 PLUS Project, College of Human Ecology, Yonsei University, Seoul 120-749, Republic of Korea
2Department of Microbiology, Hanyang University College of Medicine, Seoul 133-791, Republic of Korea

Received 8 January 2014; Accepted 16 May 2014; Published 2 June 2014

Academic Editor: Philipp M. Lepper

Copyright © 2014 Sun Eun Lee et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Helicobacter pylori is an important risk factor for gastric inflammation, which is mediated by multiple signaling pathways. The aim of this study was to investigate the effects of polyunsaturated fatty acids (PUFAs), such as linoleic acid (LA), alpha-linolenic acid (ALA), and docosahexaenoic acid (DHA), on the expression of the proinflammatory chemokine interleukin-8 (IL-8) in H. pylori-infected gastric epithelial AGS cells. To investigate whether PUFAs modulate H. pylori-induced inflammatory signaling, we determined the activation of epidermal growth factor receptor (EGFR), protein kinase C-δ (PKCδ), mitogen-activated protein kinases (MAPKs), nuclear factor-kappa B (NF-κB), and activator protein-1 (AP-1) as well as IL-8 expression in H. pylori-infected gastric epithelial cells that had been treated with or without PUFAs. We found that PUFAs inhibited IL-8 mRNA and protein expression in H. pylori-infected cells. ω-3 fatty acids (ALA, and DHA) suppressed the activation of EGFR, PKCδ, MAPK, NF-κB, and AP-1 in these infected cells. LA did not prevent EGFR transactivation and exhibited a less potent inhibitory effect on IL-8 expression than did ALA and DHA. In conclusion, PUFAs may be beneficial for prevention of H. pylori-associated gastric inflammation by inhibiting proinflammatory IL-8 expression.