title: Effects of vomitoxin ingestion on murine models for systemic lupus erythematosus.
abstract: Dietary exposure to the trichothecene vomitoxin (VT) results in reduced body weight gain, elevated serum IgA, terminal differentiation of Peyer's patch B cells to IgA secreting plasma cells haematuria, and increased kidney mesangial IgA accumulation in B6C3F1 mice and other inbred strains. These effects closely mimic a human autoimmune-like kidney disease known as IgA nephropathy. Using NZBW/F1, MRL/lpr, and BXSB mouse strains as models of systemic lupus erythematosus, we assessed whether consumption of diet containing 5 ppm or 10 ppm VT will similarly affect mice genetically prone to autoimmunity. Reduced weight gains were seen in NZBW/F1 and MRL/lpr mice fed both doses of VT within 2-3 weeks. In contrast, VT had little effect on weight gain by BXSB mice. Serum Ig levels in all three strains generally did not differ from control mice. Haematuria was significantly increased when all three strains were fed VT. In NZBW/F1 Peyer's patch cultures stimulated with lipopolysaccharide (LPS), prior VT exposure significantly increased the IgG and IgM secretion but had no effect on IgA. In MRL/lpr Peyer's patch cultures stimulated with LPS, VT exposure increased IgA secretion but not IgM or IgG. BXSB Peyer's patch cultures prepared from VT treatment groups produced significantly more IgA than controls when cultured with LPS or Concanavalin A. Whereas mesangial deposition of IgA and IgG was significantly lower in the treatment groups of NZBW/F1 and MRL/lpr mice compared with control, BXSB mice had significantly higher IgA, IgG, and complement (C3) deposition when fed VT. The results suggest that although dietary VT differentially affected mice with aberrant immune systems, these strains did not appear to be any more sensitive to the mycotoxin than were more immunologically robust inbred strains.
authors.affiliation: Department of Food Science and Human Nutrition, Michigan State University, East Lansing 48824, USA.
authors.forename: C
authors.initials: C
authors.lastname: Banotai
authors.forename: J I
authors.initials: JI
authors.lastname: Azcona-Olivera
authors.forename: D M
authors.initials: DM
authors.lastname: Greene-McDowelle
authors.forename: J J
authors.initials: JJ
authors.lastname: Pestka
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D004032:Diet; D004195:Disease Models, Animal; D005260:Female; D020022:Genetic Predisposition to Disease; D005922:Glomerulonephritis, IGA / Q000139:chemically induced; D006801:Humans; D007136:Immunoglobulins / Q000097:blood; D008180:Lupus Erythematosus, Systemic / Q000139:chemically induced*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D014255:Trichothecenes / Q000633:toxicity*; D015430:Weight Gain / Q000187:drug effects*
chemical_list: D007136:Immunoglobulins; D014255:Trichothecenes; C007262:deoxynivalenol