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      Experimental IgA Nephropathy Induced by a Low-Dose Environmental Mycotoxin, Nivalenol

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          Based on the hypothesis that IgA nephropathy (IgAN) is triggered by some exogenous antigen(s) which induces dysregulation of the mucosal immune system, we developed an experimental model of orally induced IgAN by an environmental mycotoxin, nivalenol (NIV), which often contaminates agricultural products in Southeast Asia and Japan. In the present study, low doses of oral NIV reproducibly induced significant IgA deposits in the glomerular mesangium and elevated serum IgA levels in mice irrespective of the strain; the degree of immunopathological changes analogous to human IgAN was associated with the dose and duration of NIV treatment. Furthermore, a competitive enzyme-linked immunosorbent assay with an NIV analogue-protein conjugate disclosed that the IgA antibody in the sera from the NIV model mice had a higher affinity to the mycotoxin. Conclusively, these findings suggest that NIV induces some pathological changes in mice which resemble those in human IgAN, and that this mycotoxin is associated with pathogenesis in some types of glomerulonephritis.

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          Author and article information

          S. Karger AG
          19 December 2008
          : 75
          : 4
          : 469-478
          aKidney Center, Toranomon Hospital, bOkinaka Memorial Institute for Medical Research, cDepartment of Dietetics, Otsuma Women’s College, dDepartment of Anatomy, Jikei University School of Medicine, eInstitute of Community Medicine, University of Tsukuba, fDepartment of Medicine, Tokyo Medical and Dental University, and gDepartment of Toxicology and Microbial Chemistry, Faculty of Pharmaceutical Sciences, Science University of Tokyo, Japan
          189643 Nephron 1997;75:469–478
          © 1997 S. Karger AG, Basel

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          Pages: 10
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