Rawle M. Mcintosh

Glomerular lesions produced by autologous serum and autologous IgG modified by treatment with a culture of a -haemolytic streptooccus.

Summary The theory that culture products of type-12 group A β-haemolytic streptococci may enzymically render IgG autoimmunogenic was investigated with reference to the production of an autologous immune-complex disease in rabbits. Six groups of 15 animals were used. Autologous serum that had been incubated with a culture of the test streptococcus was centrifuged and freed from bacteria by filtration and then reintroduced into the donor animals in group I. Purified autologous IgG was similarly treated with streptococcal culture and the bacteriafree material was reintroduced into the donor animals in group II. Control animals in groups III and IV were treated similarly to those in groups I and II, except that streptococci were not included in the incubation step. Animals in groups V and VI received untreated autologous serum and untreated autologous IgG respectively. Fifty per cent, of the animals in groups I and II developed haematuria and proteinuria, and showed glomerular lesions with deposition of host IgG and β1C on the basement-membranes; no streptococcal antigens could be detected in the kidney. Cultures of the injected preparations yielded no streptococci and results of blood culture and antistreptolysin O determinations were negative for all of the animals. The control animals in groups III-VI showed no abnormalities. The results of this study support the hypothesis that streptococcal modification of IgG may be related to the development of immune-deposit disease.

The Choroid Plexus: Immunologic Injury and Disease

Excerpt During the last few years it has become apparent that immunologic mechanisms are involved in cell and tissue injury in a variety of human diseases. Two immunopathogenic processes have been ...

Neuraminidase Treated Homologous IgG and Immune Deposit Renal Disease in Inbred Rats

Summary Immune deposit renal disease followed intravenous or intraperitoneal injections of neuraminidase treated homologous IgG or neuraminidase alone. No alterations were associated with several groups of controls. This preliminary study suggests that one mechanism by which microorganisms may be involved in the development of immune renal disease is by chemical alteration of immunoglobulin.

Acute and chronic effects of chemically induced unilateral renal disease in rats.

Summary Chemically induced unilateral renal disease was associated with a high incidence of proteinuria, diuresis, a morphological spectrum ranging from perinephritis to acute tubular or cortical necrosis, and unilateral or bilateral glomerular fibrinogen deposition during the first 2 wk after induction. Later, a decrease in proteinuria and return to normal urine output was not infrequently followed by recurrent proteinuria, hypergammaglobulinemia, morphological alterations, and deposition of IgG and β1C on the glomerular basement membranes and mesangium of the contra-lateral kidney and the treated kidney. Inter-capillary deposition of fibrinogen in association with IgG and β1C was occasionally observed in one or both kidneys. The morphologic, immunohistologic, serologic, and chemical findings suggest that this model may be useful for further defining the course and prognosis of unilateral renal disease produced by vascular insufficiency.

Experimental autologous immune deposit nephritis in rats associated with mercuric chloride administration

Serial administration of mercuric chloride to rats was followed by development of antibodies to tubular basement membrane and renal tubular epithelial antigen (RTE) and glomerulonephritis characterized by granular deposits of host IgG, C3 and RTE along the glomerular capillary walls. The glomerular fixed antibody was directed against RTE. These studies suggest that tubular injury by mercury may lead to release of RTE and autosensitization and subsequent antibody production to this antigen result in formation of and glomerular deposition of circulating immunopathogenic complexes (RTE-anti-RTE) and glomerular morphologic alterations.