Systhematized septal fibrosis of the liver can be induced in rats either by repeated intraperitoneal injections of pig-serum or by Capillaria hepatica infection. The relationship between these two etiological factors, as far as hepatic fibrosis is concerned, is not known, and present investigation attempts to investigate it. C. hepatica-induced septal fibrosis of the liver was considerably inhibited in rats previously rendered tolerant to pig-serum. Pig-serum-tolerant rats developed antibodies against pig-serum when infected with C. hepatica, but this did not happen when the infection occurred in normal rats. On the other hand, anti-C. hepatica antibodies failed to recognize any epitope in pig-serum, by Western blot. However, no evidence of an immunological cross reactivity was found, at least at the humoral level. Alternatively, cell-mediated mechanisms may be involved, and further investigations are warranted.

Para se investigar o potencial fibrogênico de materiais derivados da Capillaria hepatica foi feita uma tentativa para se induzir fibrose hepática septal em ratos, através de injeções intraperitoneais repetidas de um extrato de fígado de camundongo infectado pela Capillaria hepática. Dois dos 10 ratos assim tratados desenvolveram fibrose. Comparativamente, 4 dos 9 ratos que receberam injeções de soro de porco desenvolveram fibrose septal do fígado, enquanto nenhuma fibrose apareceu em 10 ratos tratados com extratos de fígado normal de camundongo. Uma vez que, na infecção natural de ratos pela Capillaria hepatica, a fibrose aparece em 100% dos casos, fica evidente que a administração intraperitoneal de uma substância não revela inteiramente o seu potencial fibrogênico.

Similarities and differences in antigenic humoral responses and electrophoretic patterns between Capillaria hepatica and pig-serum were investigated as a contribution to the understanding of hepatic fibrosis induced by the parenteral administration of foreign proteins. Only two out of 10 rats receiving repeated intraperitoneal injections of an extract of Capillaria hepatica-infected mouse liver presented septal hepatic fibrosis (20%). Under the same experimental conditions, 4 out of 9 rats (44.4%) developed septal fibrosis following whole pig-serum administration. Injections of normal mouse liver extracts did not result in hepatic fibrosis. Since a 100% septal fibrosis rate is observed in experimentally Capillaria hepatica-infected rats, it appeared that Capillaria hepatica products continuously released from inside the liver creates a much more effective fibrosis inducing mechanism than the parenteral administration of such factors. Thus, repeated peritoneal administration of a foreign protein to rats would not reveal the full fibrogenic potential it may have under natural conditions.

A fibrose septal do fígado se desenvolve regularmente em ratos infectados pela Capillaria hepatica. Com o fito de se verificar se tal tipo de fibrose também se desenvolve em camundongos, 20 animais foram infectados com 100 ou 300 ovos embrionados e examinados histologicamente em vários períodos de tempo, entre 30 até 110 dias após inoculação. Os resultados demonstraram que os camundongos desenvolvem inicialmente uma intensa hepatite aguda, difusa e focal, mas logo estas lesões são moduladas, desaparecendo a hepatite reacional difusa e persistindo as lesões em torno de ovos e restos de vermes. Alguns poucos vermes sobreviveram por todo o período experimental. Embora a fibrose perisinusoidal tenha aparecido em torno das lesões fibróticas focais, a fibrose septal não foi observada. Não se sabe por que a fibrose septal se forma no rato infectado por C. hepatica, mas não no camundongo, mas o assunto merece investigação, pois importantes aspectos da fibrogênese hepática poderiam estar implicados. Os camundongos parecem melhor adaptados à C. hepatica que os ratos; nos primeiros, a infecção é nitidamente autolimitada.

Septal fibrosis of the liver regularly develops in rats infected with Capillaria hepatica. To find out whether such fibrosis also occurs in mice, 20 animals were submitted to infection with either 100 or 300 embryonated eggs and histologically examined after several periods of time, from 30 to 110 days afterwards. Results showed that mice developed acute, severe, diffuse and focal hepatic lesions that were soon modulated to focal areas of fibrosis containing eggs and worm remnants, despite the fact that a few worms remained alive, at least up to 110 days after inoculation. Areas of perisinusoidal fibrosis appeared in the proximity and around focal parasitic lesions, but clear-cut septal fibrosis was not observed. Why septal fibrosis forms in rats, but not in mice during C. hepatica infection, only further studies can clarify. Mice seem to show better host/parasite relationship than rats in regard to C. hepatica infection.