Year-end Sale % OFF 
Abstract
Rats infected with the helminth Capillaria hepatica regularly develop septal fibrosis of the liver similar to that induced by repeated ip injections of pig serum. Fibrosis starts when the focal parasitic lesions begin to show signs of resorption, thus suggesting an immunologically mediated pathogenesis of this fibrosis. To explore this possibility, the development of C. hepatica-related hepatic fibrosis was observed in rats exposed to worm antigens from the first neonatal day onward. Wistar rats (150 g) were either injected ip with an extract of C. hepatica eggs (protein concentration: 1 mg/ml) or received immature eggs by gavage from the first neonatal day until adult life and were then infected with 500 embryonated eggs. Changes were monitored on the basis of serum levels of anti-worm antibodies and hepatic histopathology. Rats submitted to immunological oral tolerance markedly suppressed C. hepatica-related serum antibodies and septal fibrosis of the liver when infected with the helminth later on. Tolerance trials with ip injections of worm antigens gave essentially negative results. The partial suppression of septal fibrosis of the liver after the induction of immunological tolerance to C. hepatica antigens in rats indicates an immunological basis for the fibrosis and emphasizes the importance of immunological factors in the pathogenesis of hepatic fibrosis.
Highlights
Recent in vitro studies have demonstrated that soluble mediators are released by stimulated Kupffer cells [1,2,3,4], including several cytokines, such as transforming growth factor-ß [4]
Rats infected with the helminth Capillaria hepatica regularly develop septal fibrosis of the liver similar to that induced by repeated ip injections of pig serum
Rats submitted to immunological oral tolerance markedly suppressed C. hepatica-related serum antibodies and septal fibrosis of the liver when infected with the helminth later on
Summary
Recent in vitro studies have demonstrated that soluble mediators are released by stimulated Kupffer cells [1,2,3,4], including several cytokines, such as transforming growth factor-ß [4]. Bhunchet et al [12] demonstrated that pig serum acts as an antigen, with the immune response to it being the decisive factor contributing to the pathogenesis of this peculiar type of fibrosis, which proved to rest on an immunological basis. These investigators made rats tolerant to pig serum albumin by inoculating them with this protein from the first neonatal day to adult life. At the end of the tolerance induction period, the animals developed extremely low antibody levels and no evidence of hepatic fibrosis when submitted to a further period of repeated injections with pig serum albumin. This procedure resulted in high serum antibody levels and widespread hepatic septal fibrosis in nontolerant controls
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Brazilian Journal of Medical and Biological Research
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
