Selenium deficiency induced an altered immune response and increased survival following influenza A/Puerto Rico/8/34 infection.
This study was designed to determine the effect of selenium (Se) deficiency on the immune response to infection with a virulent strain of influenza virus, influenza A/Puerto Rico/8/34. Previous work in our laboratory demonstrated that Se-deficient mice infected with a mild strain of influenza virus, influenza A/ Bangkok/1/79, developed much more severe lung pathology compared with Se-adequate mice. Immune function was altered in the Se-deficient mice, and the viral genome changed to a more virulent genotype. In this study, we tested whether Se deficiency would have a similar effect on mice infected with a more virulent, mouse-adapted strain of influenza virus. Three-week-old male mice were fed Se-adequate or Se-deficient diet for 4 weeks before inoculation with influenza A/PR8/34. There was no difference in lung influenza viral titer between Se-deficient and Se-adequate mice. Se-deficient mice had less macrophage inflammatory protein 1alpha (MIP-1alpha) and regulated upon activation, normal T cell expressed and secreted (RANTES) production at the transcriptional and protein level in the lung postinfection. Se-deficient mice also had higher levels of IL-2 expression followed by a higher level of IL-4 expression in the lung. At Day 7 postinfection, there was no death in the Se-deficient group compared with 50% of the mice dying in the Se-adequate group. Sequencing of the virus isolated from infected Se-adequate and Se-deficient mice did not detect viral genome mutations in either group. This study demonstrated that Se-deficient mice had an altered immune response to an infection with a virulent strain of influenza virus. This altered immune response was beneficial for protecting the mice from influenza virus-induced mortality.
Li
Wei
W
Department of Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7461, USA.
Beck
Melinda A
MA
D000818:Animals; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000235:genetics / Q000378:metabolism; D019742:Chemokines, CC / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D009980:Influenza A virus / Q000276:immunology / Q000472:pathogenicity*; D007376:Interleukin-2 / Q000235:genetics / Q000378:metabolism; D015847:Interleukin-4 / Q000235:genetics / Q000378:metabolism; D008099:Liver / Q000201:enzymology / Q000378:metabolism; D008168:Lung / Q000378:metabolism / Q000473:pathology / Q000821:virology; D019402:Macrophage Inflammatory Proteins / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009976:Orthomyxoviridae Infections / Q000276:immunology* / Q000378:metabolism / Q000401:mortality; D012643:Selenium / Q000008:administration & dosage / Q000172:deficiency*; D016019:Survival Analysis; D015996:Survival Rate; D014774:Virulence
C496534:Ccl3 protein, mouse; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D019742:Chemokines, CC; D007376:Interleukin-2; D019402:Macrophage Inflammatory Proteins; D015847:Interleukin-4; D005979:Glutathione Peroxidase; D005978:Glutathione; D012643:Selenium