Selenoprotein P is not essential for an effective immune response to influenza infection in mice

Abstract

We have demonstrated previously that Se deficiency impairs the antiviral cytokine response to influenza infection. Previous work with the antioxidant glutathione peroxidase 1 knockout mice suggests a role for this selenoprotein in the immune function. Because selenoprotein P has been postulated to prevent oxidant injury in the extracellular space as well as providing transport for Se to tissues, we investigated its role in the immune response to influenza virus infection. Male and female selenoprotein P knockout (SelP −/−) on a 1ppm Se diet and wildtype (WT) controls were infected with influenza A/PR8 and sacrificed at 0, 3 and 6 days post infection. Lung mRNA levels were elevated for innate, pro-inflammatory and T-cell cytokines, as well as chemokines in response to infection. However, there was no difference in the magnitude of the response between the SelP −/− and WT mice. Additionally, there was no difference in lung pathology between the two groups at any time point post infection. In order to determine what role anti-oxidant enzymes may play in this model, livers were analyzed for glutathione peroxidase-1, thioredoxin reductase, catalase, and superoxide dismutase activity. There were no differences in activity in any of these enzymes between the groups of mice at any time point. Together, these data indicate that SelP is not essential for the immune response to influenza virus and that an increase in anti-oxidant enzymes does not accompany influenza infection of SelP −/− mice. Supported byNIH grant R01 AI055050 to MAB.