The aim of this study was to test the anti-fibrotic effect of interferon in this experimental model. Treatment with interferon- a proved to inhibit the development of fibrosis in this model, especially when doses of 500,000 and 800,000 IU were used for 60 days. Nevertheless, it remains rather difficult to determine from such clinical studies whether the effect on fibrosis was indeed direct or merely secondary to modulatory and anti-viral properties of the drug. As a contribution to this subject, the present paper deals with the effects of interferon- a on a new model of hepatic fibrosis in rats. Septal fibrosis starts one month after infection and is already well developed around the 40th day, when the worms have already died and the focal direct parasite-dependent lesions exhibit encapsulation and signs of progressive resorption.
Septal fibrosis is progressive from then on, and the late outcome is a full picture of cirrhosis.
Moreover, similar to the pig-serum model, septal fibrosis in capillariasis is not preceded by diffuse chronic inflammation or overt hepatocellular necrosis. Antigenic materials sequestered within the focal parasitic lesions, being slowly released during prolonged periods of time, have been suspected as the main pathogenic factor in hepatic fibrosis associated with C. hepatica infection in rats.