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Nutritional Immunology

Decreased Selenoprotein Expression Alters the Immune Response during Influenza Virus Infection in Mice^1–3,

⁴ Department of Nutrition, University of North Carolina, Chapel Hill, NC 27599; ⁵ Molecular Biology of Selenium, National Cancer Institute, NIH, Bethesda, MD 20892; and ⁶ Laboratory of Animal Science Program, Science Applications International Corporation-Frederick, Inc., National Cancer Institute, Frederick, MD 21702

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

Previous work from our laboratory demonstrated that host selenium (Se) deficiency results in greater lung pathology and altered immune function in mice infected with influenza virus. Because selenoproteins play a key role in determining the oxidant status of the host, we utilized a transgenic mouse line carrying a mutant selenocysteine (Sec) tRNA ^[Ser]Sec transgene (t-trspi⁶A^–). The levels of selenoproteins are decreased in these mice in a protein- and tissue-specific manner. Male t-trspi⁶A^– and wild-type (WT) mice were infected with influenza and killed at various time points postinfection (p.i.). Lung mRNA levels for innate and pro-inflammatory cytokines increased with infection but did not differ between groups. However, at d 2 p.i., chemokine levels were greater in the t-trspi⁶A^– mice compared with WT mice. Additionally, IFN- was higher at d 7 p.i. in the t-trspi⁶A^– mice and viral clearance slower. Despite these immune system changes, lung pathology was similar in t-trspi⁶A^– and WT mice. ⁷⁵Se labeling experiments demonstrated that glutathione peroxidase (GPX)-1 and thioredoxin reductase, although greatly diminished in the lungs of t-trspi⁶A^– mice, were not altered as a result of infection. GPX-1 activity in the lungs of the t-trspi⁶A^– mice was 82% of the WT mice. In addition, the GPX-1 activity in the lungs of Se-deficient mice was 125% less than in the t-trspi⁶A^– mice. These results suggest that although selenoproteins are important for immune function, there is a threshold of GPX-1 activity that can prevent an increase in lung pathology during influenza infection.

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