The research investigated the combined effects of protein deficiency (PD) and a gastrointestinal nematode infection, Heligmosomoides bakeri , on immunopathology and nutritional status in BALB/c mice. The acute phase of a primary infection reduced resting metabolic rate, but PD did not. Early challenge infection led to temporary anorexia and cessation of weight gain in both protein-sufficient (PS) and PD mice. / Among PS mice, a challenge dose of 200 L3 caused more active worm expulsion than infection with 100 L3. Both serum monocyte chemotactic protein-5 and gut fluid leakage were positively correlated with worm expulsion whereas numbers of mucosal mast cells, eosinophils, goblet cells and Paneth cells were unaffected by doses. Among PD mice, worm survival was prolonged and no dose-dependent worm expulsion was observed. In addition, a wide range of Th1 inflammatory cytokines including leptin was elevated in infected PD mice suggesting (1) that PD mice are unable to mount the appropriate Th2 inflammation and (2) that infection in PD mice induces a Th1 inflammation that allows continuing persistence of the parasite. / The shift to Th1 inflammatory responses in PD mice may also explain modifications in mineral distributions in tissues. Despite adequate dietary intakes of minerals in both PD and PS mice, serum iron concentrations were lower after H. bakeri challenge infection. Infection also reduced calcium and iron concentrations as well as the Ca/Zn ratio in the spleen. In contrast, PD resulted in increased iron and calcium concentrations as well as increased Ca/Zn ratio in the spleen and Fe/Zn ratio in the liver, but reduced calcium, zinc, copper and sulfur concentrations, and the Cu/Zn ratio in the liver. / Re-feeding PD mice with a PS diet restored parasite expulsion, regardless of whether the PS diet was provided during the primary or challenge infection. Thus, although PD mice have suppressed Th2 responses and elevated Th1 inflammation, their response to the primary infection is sufficient to ensure that parasite expulsion occurs once protein status is restored. / Together, these studies show that the shift toward Th1 inflammation plays a key role in prolonged parasite survival and mineral redistribution in protein deficient, infected mice.
| Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.115906 |
| Date | January 2008 |
| Creators | Tu, Tao, 1971- |
| Publisher | McGill University |
| Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
| Language | English |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Format | application/pdf |
| Coverage | Doctor of Philosophy (School of Dietetics and Human Nutrition.) |
| Rights | All items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated. |
| Relation | alephsysno: 002837813, proquestno: AAINR66700, Theses scanned by UMI/ProQuest. |
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