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IgA-IgG disease in the intestine of Brown-Norway rats ingesting mercuric chloride
In Brown-Norway (BN) rats, oral administration of mercuric chloride (HgCl2) induced morphological lesions of the ileum and, in lesser degree, of the colon, with abnormal deposits of IgA in the basement membranes of intestinal glands and of IgG in the basement membranes and in the lamina propria. IgG reactive with renal and intestinal basement membranes and in the lamina propria. IgG reactive with renal and intestinal basement membranes and with the lamina propria of a normal BN rat was found in the serum and IgG deposits were present in renal glomeruli of BN rats receiving HgCl2. Thus, it is conceivable that the deposits of IgG present in the intestine resulted from local fixation of circulating autoantibodies. In contrast, IgA with basement membrane reactivity was not detected in the sera nor in the renal glomeruli, suggesting that the intestinal deposits of IgA were formed in situ. This IgA-IgG intestinal disease inducible in BN rats may provide a model for the study of alterations of the secretory IgA system, as well as for testing the possibility that abnormal deposits IgA-IgG in the intestinal structures are associated with local functional changes.
In Brown-Norway (BN) rats, oral administration of mercuric chloride (HgCl2) induced morphological lesions of the ileum and, in lesser degree, of the colon, with abnormal deposits of IgA in the basement membranes of intestinal glands and of IgG in the basement membranes and in the lamina propria. IgG reactive with renal and intestinal basement membranes and in the lamina propria. IgG reactive with renal and intestinal basement membranes and with the lamina propria of a normal BN rat was found in the serum and IgG deposits were present in renal glomeruli of BN rats receiving HgCl2. Thus, it is conceivable that the deposits of IgG present in the intestine resulted from local fixation of circulating autoantibodies. In contrast, IgA with basement membrane reactivity was not detected in the sera nor in the renal glomeruli, suggesting that the intestinal deposits of IgA were formed in situ. This IgA-IgG intestinal disease inducible in BN rats may provide a model for the study of alterations of the secretory IgA system, as well as for testing the possibility that abnormal deposits IgA-IgG in the intestinal structures are associated with local functional changes.