title: Anti-inflammatory effects of long-chain n-3 PUFA in rhinovirus-infected cultured airway epithelial cells.
abstract: Long-chain n-3 PUFA (LCn-3PUFA) including DHA and EPA, are known to decrease inflammation by inhibiting arachidonic acid (AA) metabolism to eicosanoids, decreasing the production of pro-inflammatory cytokines and reducing immune cell function. The aim of this study was to determine if EPA and DHA reduced the release of inflammatory mediators from airway epithelial cells infected with rhinovirus (RV). Airway epithelial cells (Calu-3) were incubated with EPA, DHA and AA for 24 h, followed by rhinovirus infection for 48 h. IL-6, IL-8 and interferon-gamma-induced protein-10 (IP-10) released by cells were measured using ELISA. Viral replication was measured by serial titration assays. The fatty acid content of cells was analysed using GC. Cellular viability was determined by visual inspection of cells and lactate dehydrogenase release. DHA (400 microm) resulted in a significant 16% reduction in IL-6 release after RV-43 infection, 29% reduction in IL-6 release after RV-1B infection, 28% reduction in IP-10 release after RV-43 infection and 23 % reduction in IP-10 release after RV-1B infection. Cellular DHA content negatively correlated with IL-6 and IP-10 release. None of the fatty acids significantly modified rhinovirus replication. DHA supplementation resulted in increased cellular content of DHA at the cost of AA, which may explain the decreased inflammatory response of cells. EPA and AA did not change the release of inflammatory biomarkers significantly. It is concluded that DHA has a potential role in suppressing RV-induced airway inflammation.
authors.affiliation: Nutraceuticals Research Group, School of Biomedical Sciences, University of Newcastle, Newcastle, NSW, Australia.
authors.forename: Ahmad
authors.initials: A
authors.lastname: Saedisomeolia
authors.forename: Lisa G
authors.initials: LG
authors.lastname: Wood
authors.forename: Manohar L
authors.initials: ML
authors.lastname: Garg
authors.forename: Peter G
authors.initials: PG
authors.lastname: Gibson
authors.forename: Peter A B
authors.initials: PA
authors.lastname: Wark
mesh_terms: D000704:Analysis of Variance; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D016718:Arachidonic Acid / Q000378:metabolism; D002460:Cell Line; D054357:Chemokine CXCL10 / Q000032:analysis; D004281:Docosahexaenoic Acids / Q000032:analysis / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D015118:Eicosapentaenoic Acid / Q000032:analysis / Q000494:pharmacology; D004847:Epithelial Cells / Q000187:drug effects / Q000276:immunology / Q000821:virology*; D015525:Fatty Acids, Omega-3 / Q000627:therapeutic use*; D006801:Humans; D015850:Interleukin-6 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D010850:Picornaviridae Infections / Q000188:drug therapy* / Q000276:immunology; D020545:Respiratory Mucosa / Q000187:drug effects / Q000276:immunology / Q000821:virology*; D012229:Rhinovirus
chemical_list: D000893:Anti-Inflammatory Agents; C114753:CXCL10 protein, human; D054357:Chemokine CXCL10; D015525:Fatty Acids, Omega-3; D015850:Interleukin-6; D016209:Interleukin-8; D004281:Docosahexaenoic Acids; D016718:Arachidonic Acid; D015118:Eicosapentaenoic Acid