|Shea Donohue, P|
Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/5/2005
Publication Date: 3/18/2005
Citation: Smith, A.D., Madden, K. B., Au Yeung, K., Zhao, A., Elfrey, J., Finkelman, F., Levander, O.A., Shea Donohue, P.T., and Urban Jr, J.F. 2005. Effect of selenium and/or vitamin E deficiencies on Heligmosomoides polygyrus infections in mice. Journal of Nutrition. 135:830-836.
Interpretive Summary: Previous studies have shown that deficiencies in nutrients such as selenium (Se) and/or vitamin E (VE) can alter the normal course of infection by common viruses including influenza. Both Se and VE are known to be important for proper immune function. Intestinal worms commonly infect over one quarter of the world's population, although the heaviest infections are in countries with poor sanitation and health care. These populations often have the confounding factor of poor nutrition. A study was conducted with Heligmosomoides polygyrus, a worm that naturally infects mice, to determine if nutrition, and specifically dietary deficiencies in Se and/or VE could alter the response to a worm infection. Mice deficient in Se and/or VE were unable to adequately expel worms from the intestines and the worms had egg production which facilitates greater infectivity. The intestinal tract normally responds to worm infections by increasing the amount of fluid to help flush the worms out. Mice double deficient in Se and VE did not have this normal response but other intestinal messenger molecules that trigger expulsion of worms were normal. These results describe an important role for both Se and VE in the protective response to worm infections and show that there are distinct tissue targets that can lead to a suboptimal response to infection. The impact of these results is the description of a unique role for selenium and vitamin E in worm infections and that adequate micronutrient levels are needed to support optimal immune function.
Technical Abstract: Previous studies have shown that selenium (Se) and/or vitamin E (VE) deficiencies can alter the pathogenesis of coxsackievirus B3 and influenza viral infections. Both Se and VE are known to play a role in immune function and in antioxidant defense. To determine if deficiencies in Se and/or VE could impact the normal course of a Heligmosomoides polygyrus infection, mice were made deficient in Se and/or VE and infected with H. polygyrus. Both the primary and secondary infections, administered to drug-cured mice, were assessed. The primary H. polygyrus infection was unaffected by diet. In contrast, Se, VE, and Se/VE double deficiencies all caused delayed worm expulsion and increased fecundity in secondary infections suggesting impairment of the normal clearance response to infection. Systemic IL-4 production in response to infection was not altered by diet. Se/VE double deficiency prevented the H. polygyrus-induced decrease in gastrointestinal sodium-dependent glucose absorption but had no effect on the increase in epithelial cell permeability normally seen in response to H. polygyrus infection. The results presented here describe an important role for both Se and VE in the protective response to secondary H. polygyrus infections.