Murine alveolar hydatidosis: a potential experimental model for the study of AA-amyloidosis.

Histochemical and immunohistologic evidence has been presented to characterize the AA-type of amyloidosis in C57BL/6J (H-2b) mice infected i.p. with 50 cysts of Echinococcus multilocularis. Congo red-stained sections of kidneys and spleens from 4 weeks postinfected (p.i.) hydatid-mice were negative for the amyloid deposits. Heavy amyloid deposits, which in ultrathin sections of kidneys measured 8-12 nm in thickness, obliterated the perifollicular sinuses in spleens and glomerular capillaries in kidneys at 16 weeks p.i. Amyloid deposits were resistant to potassium permanganate treatment. They bind strongly to rabbit anti-mouse AA serum (RAA) as demonstrated by using peroxidase-anti-peroxidase technique. Preabsorption of RAA with azo-casein induced amyloid abolished completely the binding of RAA to mouse AA and hydatid-mouse deposits. Rabbit monospecific mouse antisera to heavy and light chains of Igs did not bind to amyloid deposits in hydatid-mice kidneys. Enumeration of spleen cells from the 16 weeks p.i. amyloidotic spleens showed a significant reduction in the total lymphocytes and T-cells. Overt accumulation of amyloid deposits in the spleen was associated with its disorganization, a significant reduction in T-cells and the depressed response of spleen cells to ConA and LPS mitogens. The relationship between proliferating alveolar hydatid cyst, intense inflammatory response, depressed cell mediated immunity and AA-type of amyloidosis is discussed in murine hydatidosis.