Ultrastructural studies of experimental autoimmune glomerulonephritis in normal and bursectomized chickens

Immunizations of chickens with bovine glomerular basement membrane (GBM) results in the development of experimental autoimmune glomerulonephritis (EAG). Animals lacking antibody to GBM develop nephritis comparable to those with antibody. The present study examined the ultrastructural lesions of EAG. Normal and bursectomized (Bsx) chickens were immunized with complete Freund's adjuvant (CFA) or CFA-GBM. We studied 3 CFA controls, 5 CFA-Bsx controls, 5 GBM immunized, 4 Bsx-GBM immunized antibody positive birds, and 6 Bsx-GBM immunized birds with no antibody. Ultrastructure of control animals was consistent with previous descriptions in chickens. In nephritic GBM-immunized animals the proliferative glomerulonephritis was associated with an increase in resident mesangial (type I) cells identified by small regularly shaped nuclei with coarsely clumped chromatin and scanty cytoplasm. (p less than 0.05). Glomerulonephritis was also associated with the occurrence of type II cells characterized by an irregular folded lobulated nucleus, finely granular chromatin, abundant cytoplasm, and dense granules and vacuoles in the cytoplasm with an appearance similar to macrophages. The presence of type II cells was highly associated with the development of glomerulonephritis, p less than 0.05. The increase in type II cells was observed in animals with and without antibody along the GBM. A third type of cell was also observed in intimate contact with type II cells and had the morphology of a lymphocyte. The lymphocytoid cells were only seen in nephritic animals. Bsx was associated with trabeculation and lucencies of the GBM not found in normal birds, p less than 0.05. EAG in chickens occurs regardless of the presence or absence of GBM-bound anti-GBM antibody. Other studies have shown that the disease can be transferred by specifically sensitized lymphocytes, but not by antibody. The present ultrastructural findings provide further evidence for the role of cell mediated immunity in the pathogenesis of this model of EAG in chickens.