Splenomegaly and immune complex splenitis in rabbits with experimentally induced chronic serum sickness: immunopathological findings.

Abstract

This study describes the morphological and immunocytochemical aspects of the spleen in rabbits with experimentally induced chronic serum sickness. Thirty-seven rabbits were immunized with daily injections of bovine serum albumin (BSA) and six served as non-immunized controls. The most significant lesions were found in rabbits with chronic serum sickness induced by high doses of BSA. The spleens were increased in size and in weight. Granular deposits of BSA, rabbit IgG and C3, presumably immune complexes (IC), were found in the basement membranes of the venous sinuses and of the capillaries in the marginal zone, in the walls of splenic arterioles and, occasionally, between the macrophages in the splenic cords and lymphoid cells in lymphatic follicles. An increased number of degranulated polymorphonuclear leukocytes, macrophages and giant cells, degenerative changes of dendritic cells and, in some instances, splenic fibrosis were also seen. These splenic lesions developed when the concentration of BSA-antibodies in the sera decreased. The spleens of rabbits receiving high doses of BSA in a stage between acute and chronic serum sickness were also increased in size and in weight. The red pulp was enlarged, and immune deposits were observed within macrophages but not in splenic structures. The spleens of non-responder rabbits had a slight decrease in number of lymphatic follicles and germinal centers only. The spleens of non-immunized rabbits were consistently normal. The results indicate that in rabbits receiving multiple injections of high doses of BSA, chronic serum sickness is associated with splenomegaly and IC-splenitis and that these lesions occur when the level of circulating BSA antibody declines. IC-splenitis could impair the clearance of IC and influence the immune function of the spleen. These findings could have implications in the pathogenesis of splenomegaly and of defective splenic function in human IC-mediated diseases.