Rapid deposition of glomerular IgA in BALB/c mice by nivalenol
Exp Toxicol Pathol. 2009 Sep 26.
Dewa Y, Kemmochi S, Kawai M, Saegusa Y, Harada T, Shimamoto K, Mitsumori K,
Kumagai S, Sugita-Konishi Y, Shibutani M.
Laboratory of Veterinary Pathology, Tokyo University of Agriculture and
Technology, 3-5-8 Saiwai-cho, Fuchu-shi, Tokyo 183-8509, Japan; Pathogenetic
Veterinary Science, United Graduate School of Veterinary Sciences, Gifu
University, 1-1 Yanagido, Gifu 501-1193, Japan.
To clarify the underlying mechanisms of IgA nephropathy (IgAN) induced by
nivalenol , a trichothecene mycotoxin, we examined the time and dose
relationships of glomerular deposition of IgA by nivalenol in BALB/c mice
(Experiment 1), and also evaluated the modification of nivalenol on spontaneous
IgAN in an inbred murine model, a high IgA strain (HIGA), during its early stage
of pathogenesis (Experiment 2). In Experiment 1, female BALB/c mice were given a
diet containing 0, 12, or 24ppm concentration of nivalenol for 4 or 8 weeks. An
increase in serum IgA levels was found at 24ppm from 4 weeks. At week 8 of
treatment, dose-dependent increases in serum IgA levels and glomerular
deposition of IgA and IgG were observed without accompanying histopathological
glomerular changes. On the other hand, in Experiment 2, control HIGA mice
exhibited rather high levels of serum IgA as compared with BALB/c mice from 4
weeks of experiment as well as glomerular deposition of IgA and IgG and
mesangial proliferation as revealed at week 8. nivalenol at 24ppm further
increased serum IgA in this strain; however, it did not enhance glomerular
immunoglobulin deposition or histopathological lesion. These results suggest
that NIV-induced increase of serum IgA levels may be primarily responsible for
glomerular immunoglobulin deposition; however, nivalenol does not enhance
glomerular IgA deposition that may lead to exacerbation of predisposed IgAN in
the short term, irrespective of the further elevation of serum IgA from the high
basal levels.
PMID: 19783131
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