|Shea Donohue, P|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 11/13/2003
Publication Date: 3/24/2004
Citation: Smith, A.D., Madden, K., Zhao, A., Auyeung, K., Levander, O.A., Finkelman, F., Urban Jr, J.F., Shea Donohue, P.T. 2004. Selenium (se) and vitamin E (ve) deficiencies impair intestinal function and result in persistent infection with heligmosomoides polygyrus [abstract]. Federation of American Society of Experimental Biology Journal. 18(4):A9. Interpretive Summary:
Technical Abstract: Intestinal nematode parasites are responsible for significant morbidity world-wide especially in malnourished populations that express limited immunity and poor worm clearance. Selenium (Se) and vitamin E (VE) deficiencies are likely in the malnourished and contribute to increased pathogenesis following infection with coxsackie- or influenza virus and the protozoan Trypanasoma cruzi, but have not been studied following a nematode infection. Mice infected with the intestinal nematode Heligmosomoides polygyrus (Hp) exhibit a chronic infection that when drug-cleared induces a memory response to a challenge infection characterized by enhanced immune clearance associated with decreased intestinal epithelial cell glucose absorption, increased mucosal permeability, and enhanced smooth muscle contractility. Both Se and/or VE deficiencies resulted in increased worm persistence and egg production during a memory response compared to mice fed an adequate diet. The characteristic increase in serum IL-4 levels was observed in all Hp-infected mice regardless of diet; however, the pattern of decreased glucose absorption and increased smooth muscle contractility was impaired in VE but not Se deficient mice in spite of diet-independent changes in Hp-induced mucosal permeability and Cl- secretion. These results suggest that Se and VE deficiencies impair the host intestinal memory response to Hp infection via two different mechanisms.