British Journal of Nutrition

Full Papers

Nutritional Immunology

Anti-inflammatory effects of long-chain n-3 PUFA in rhinovirus-infected cultured airway epithelial cells

Ahmad Saedisomeoliaa1a2, Lisa G. Wooda2a3a4 c1, Manohar L. Garga1, Peter G. Gibsona2a3a4 and Peter A. B. Warka2a3a4

a1 Nutraceuticals Research Group, School of Biomedical Sciences, University of Newcastle, Newcastle, NSW, Australia

a2 Respiratory and Sleep Medicine, Hunter Medical Research Institute, John Hunter Hospital, Newcastle, NSW, Australia

a3 School of Medicine and Public Health, University of Newcastle, Newcastle, NSW, Australia

a4 Centre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Newcastle, NSW, Australia

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-γ-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 μm) 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.

(Received February 19 2008)

(Revised May 21 2008)

(Accepted May 22 2008)

(Online publication July 17 2008)

Correspondence:

c1 Corresponding author: Dr Lisa G. Wood, fax +61 2 49855850, email lisa.wood@newcastle.edu.au

Footnotes

Abbreviations: AA, arachidonic acid; 10 % FCS/MEM, minimum essential medium containing 10 % fetal calf serum; IP-10, interferon-γ-induced protein-10; LCn-3PUFA, long-chain n-3 PUFA; RV, rhinovirus; TCID50, tissue culture infectious dose at 50 %; TLR, toll-like receptor

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