AN EXPERIMENTAL-MODEL FOR ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS IN MICE

A number of factors have been implicated in the pathogenesis of acute poststreptococcal glomerulonephritis (APSGN). The lack of a reliable a nimal model has made it difficult to further examine the role of these factors in the pathogenetic process. In this report, we present a tis sue cage model in mice for the study of APSGN. Morphological and immun ohistological changes in the kidney, resembling those of APSGN in man, were induced at high frequency in the experimental model after infect ion with group A streptococcal nephritis isolates. Nephritis-associate d strains induced hypercellularity, occlusion of capillaries, and C3 d eposition at high frequencies compared to the changes induced in anima ls infected with a non-nephritis-associated strain and non-infected co ntrols. In animals infected with a nephritis isolate, hematuria and pr oteinuria were also detected. If penicillin treatment was initiated on the third day of infection, the development of the nephritis process was prevented. Streptokinase, as well as preabsorbing antigen and stre ptococcal pyrogenic exotoxin B (SpeB), have been implicated in the pat hogenesis of APSGN. These proteins, as well as SpeA and SpeF, were det ected in the fluids of the infectious focus, regardless of the origin of the strains and whether or not glomerulonephritis was seen. Antibod ies to streptokinase were evoked in the majority of the infected anima ls. This immune response did not correlate with the nephritic process since hypercellularity was also seen in animals which lacked detectabl e streptokinase antibodies. The results show that the mouse tissue cag e model can be used to study APSGN and to evaluate factors involved in the pathogenesis of the disease.