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Selenium (Se) deficiency alters intestinal diaphorase activity in mice infected with the intestinal parasitic worm Heligmosomoides polygyrus
Author(s) -
Urban Joseph F.,
Smith Allen,
Botero Sebastian,
Dawson Harry,
Anthony Robert,
Gause William,
SheaDonohue Terez
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a63-a
Subject(s) - heligmosomoides polygyrus , selenium deficiency , biology , immune system , immunology , nematode , endocrinology , oxidative stress , catalase , ecology , glutathione peroxidase
Mice fed a diet deficient in Se show reduced resistance to a secondary infection with H. polygyrus . IL‐4 and IL‐13 dependent increases in intestinal smooth muscle hyper‐contractility and decreased glucose absorption correlate with expulsion of the adult worm following a challenge infection. Selenium deficiency, however, does not affect local intestinal gene expression for IL‐4 and IL‐13 or associated changes in smooth muscle and epithelial cell function. This suggests another protective mechanism compromised by Se deficiency. Parasitic H. polygyrus larvae encyst in the submucosa of the duodenum prior to development of the luminal dwelling adult stage. Neutrophils and alternatively activated macrophages (AAM) surround the larval stage, and inactivation of AAM activity contributes to greater susceptibility to infection. Selenium deficiency appears not to affect AAM infiltration around the larvae, but does reduce NADPH diaphorase activity. This suggests a role for Se in localized oxidants important for host defense.