title: Anti-inflammatory mechanism of polyunsaturated fatty acids in Helicobacter pylori-infected gastric epithelial cells.
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 (PKC δ), 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, PKC δ, 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.
authors.affiliation: Department of Food and Nutrition, Brain Korea 21 PLUS Project, College of Human Ecology, Yonsei University, Seoul 120-749, Republic of Korea.
authors.forename: Sun Eun
authors.identifier: 0000-0002-1983-4561
authors.initials: SE
authors.lastname: Lee
authors.affiliation: Department of Food and Nutrition, Brain Korea 21 PLUS Project, College of Human Ecology, Yonsei University, Seoul 120-749, Republic of Korea.
authors.forename: Joo Weon
authors.initials: JW
authors.lastname: Lim
authors.affiliation: Department of Microbiology, Hanyang University College of Medicine, Seoul 133-791, Republic of Korea.
authors.forename: Jung Mogg
authors.initials: JM
authors.lastname: Kim
authors.affiliation: Department of Food and Nutrition, Brain Korea 21 PLUS Project, College of Human Ecology, Yonsei University, Seoul 120-749, Republic of Korea.
authors.forename: Hyeyoung
authors.initials: H
authors.lastname: Kim
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002460:Cell Line; D004847:Epithelial Cells / Q000166:cytology / Q000187:drug effects* / Q000382:microbiology*; D066246:ErbB Receptors / Q000378:metabolism; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005231:Fatty Acids, Unsaturated / Q000494:pharmacology*; D005753:Gastric Mucosa / Q000166:cytology*; D016480:Helicobacter pylori / Q000187:drug effects* / Q000472:pathogenicity*; D006801:Humans; D016209:Interleukin-8 / Q000235:genetics; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D011493:Protein Kinase C / Q000378:metabolism; D000099221:Protein Kinase C zeta
chemical_list: D000893:Anti-Inflammatory Agents; D066246:ErbB Receptors; D048049:Extracellular Signal-Regulated MAP Kinases; D005231:Fatty Acids, Unsaturated; D016209:Interleukin-8; D048031:JNK Mitogen-Activated Protein Kinases; D011493:Protein Kinase C; D000099221:Protein Kinase C zeta; C512478:EGFR protein, human