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J. Nutr. First published June 23, 2009; doi:10.3945/jn.109.108027
Journal of Nutrition, doi:10.3945/jn.109.108027
Vol. 139, No. 8, 1588-1594, August 2009

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© 2009 American Society for Nutrition


Nutritional Immunology

Fish Oil-Fed Mice Have Impaired Resistance to Influenza Infection1,2

Nicole M. J. Schwerbrock, Erik A. Karlsson, Qing Shi, Patricia A. Sheridan and Melinda A. Beck3,*

Department of Nutrition, The University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599

Dietary fish oils, rich in (n-3) PUFA, including eicosapentaenoic acid and docosahexaenoic acid, have been shown to have antiinflammatory properties. Although the antiinflammatory properties of fish oil may be beneficial during a chronic inflammatory illness, the same antiinflammatory properties can suppress the inflammatory responses necessary to combat acute viral infection. Given that (n-3) fatty acid-rich fish oil supplementation is on the rise and with the increasing threat of an influenza pandemic, we tested the effect of fish oil feeding for 2 wk on the immune response to influenza virus infection. Male C57BL/6 mice fed either a menhaden fish oil/corn oil diet (4 g fish oil:1 g corn oil, wt:wt at 5 g/100 g diet) or a control corn oil diet were infected with influenza A/PuertoRico/8/34 and analyzed for lung pathology and immune function. Although fish oil-fed mice had lower lung inflammation compared with controls, fish oil feeding also resulted in a 40% higher mortality rate, a 70% higher lung viral load at d 7 post infection, and a prolonged recovery period following infection. Although splenic natural killer (NK) cell activity was suppressed in fish oil-fed mice, lung NK activity was not affected. Additionally, lungs of infected fish oil-fed mice had significantly fewer CD8+ T cells and decreased mRNA expression of macrophage inflammatory protein-1-{alpha}, tumor necrosis factor-{alpha}, and interleukin-6. These results suggest that the antiinflammatory properties of fish oil feeding can alter the immune response to influenza infection, resulting in increased morbidity and mortality.


* To whom correspondence should be addressed. E-mail: melinda_beck{at}unc.edu.

Manuscript received 30 March 2009. Initial review completed 14 April 2009. Revision accepted 29 May 2009.

Published online 23 June 2009.







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