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Nutritional Immunology

Deficiencies in Selenium and/or Vitamin E Lower the Resistance of Mice to Heligmosomoides polygyrus Infections

Allen Smith^*, Kathleen B. Madden, Karla J. Au Yeung^**, Aiping Zhao, Justin Elfrey, Fred Finkelman, Orville Levander^*, Terez Shea-Donohue^*, and Joseph F. Urban, Jr.^*,1

^* Nutrient Requirements and Functions Laboratory, Beltsville Human Nutrition Research Center, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, MD; Department of Pediatrics and Department of Medicine, Uniformed Services University of Health Sciences, Bethesda, MD; ^** Department of Pediatrics, Walter Reed Army Medical Center, Washington, DC; and University of Cincinnati College of Medicine, Cincinnati Children’s Hospital Medical Center, and Cincinnati Veterans Administration Medical Center, Cincinnati, OH

¹To whom correspondence should be addressed. E-mail: urbanj{at}ba.ars.usda.gov.

Previous studies have shown that deficiencies in selenium (Se) and/or vitamin E (VE) can exacerbate the infectivity and pathogenesis of coxsackievirus B3 and influenza. Both Se and VE play a role in immune function and antioxidant defense. To determine whether these deficiencies would affect the normal course of infection with a metazoan parasite, mice were made deficient in Se and/or VE and inoculated with the gastrointestinal nematode parasite Heligmosomoides polygyrus. Both primary and secondary infections were assessed. Although the course of a primary infection with H. polygyrus was unaffected by diet, diets deficient in Se, VE, and both Se and VE (Se/VE double-deficiency) all caused delayed adult worm expulsion and increased fecundity during a secondary infection; suggesting an impaired intestinal response. H. polygyrus-induced IL-4 levels were diet-independent; but Se/VE double-deficiency blocked the H. polygyrus-induced IL-4 receptor-associated decrease in sodium-dependent glucose absorption in the jejunum that contributes to worm expulsion. In contrast, Se/VE double-deficiency had no effect on the infection-induced, IL-4R-associated increase in epithelial cell permeability that accompanies the infection. These results suggest that both Se and VE are required for specific IL-4-related changes in intestinal physiology that promote host protection against H. polygyrus.

KEY WORDS: • selenium • vitamin E • parasite • immunity • gastrointestinal

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