BACKGROUND. Post-streptococcal glomerulonephritis (PSGN) refers to the sequela of the acute infection, caused by Streptococcus pyogenes. The pathology has been studied for a long time, and today attempts are being made to identify the products of their life activity, able to initiate an immunopathological process in kidneys. Most attention is given to IgGFc-binding proteins and streptokinase, the enzyme transforming blood plasminogen into plasmin. The aim of this investigation was to study the role IgGFc-binding proteins and streptokinase in the development of glomerulonephritis in rabbits.
MATERIAL AND METHODS. GAS strains of M types 1, 12, 22 and their ska- isogenic mutants were used in the study. To reproduce PSGN tissue cages were implanted to rabbit under their skin; after the complete healing of the wounds the animals were infected with “alive” streptococci and observed for three weeks. By the end of the term, the kidneys of the survived rabbits were subjected to immunohistological analysis.
RESULTS. In experiments on PSGN induction in rabbits, we failed to detect streptokinase involvement, because no differences between the initiation of glomerulonephritis by wild strains or by ska- isogenic mutants were identified. Mutant strains deficient in the gene responsible for the synthesis of streptokinase but having retained ability to bind rabbit and human IgG, caused morphological changes in kidney tissue, specific for PSGN.
CONCLUSION. Comparative analysis of “rabbit” and “mouse” models of PSGN, developed by the same technology, led to opposing conclusions concerning the role of streptokinase in pathogenesis of experimental glomerulonephritis. The role of IgGFc-binding activity of GAS in the development of experimental PSGN is discussed.