RESUMO
We have examined the role of inflammatory cells, ischemia and serum complement on the development of acute experimental amoebic liver abscess in hamsters (AEALAH). In hamsters made leukopenic by whole body radiation (800 rad) and daily intraperitoneal glycogen injections, the absence of inflammatory cells and liver tissue damage surrounding the parasites resulted in their rapid (24 h) disappearance from the liver, which showed no lesions. Focal liver ischemia, always present in control AEALAH with inflammation and tissue destruction, was reproduced in radiated hamsters by injection of amoebae mixed with Superdex microspheres, but again in the absence of inflammation, amoebae caused no liver damage and disappeared in 24 h. In hamsters made hypocomplementemic by injection of purified cobra venom factor (CVF), amoebae caused AEALA indistinguishable from controls, but in leukopenic + hypocomplementemic hamsters, amoebae were unable to produce lesions and disappeared from the liver in 48 h. We conclude that inflammation and tissue damage are required for the survival of amoebae in AEALAH and for the progression of the experimental disease.
Assuntos
Proteínas do Sistema Complemento/imunologia , Entamoeba histolytica/fisiologia , Hepatite/patologia , Isquemia/patologia , Abscesso Hepático Amebiano , Fígado/patologia , Doença Aguda , Animais , Proteínas Inativadoras do Complemento/farmacologia , Modelos Animais de Doenças , Venenos Elapídicos/farmacologia , Entamoeba histolytica/efeitos da radiação , Feminino , Cobaias , Hepatite/imunologia , Hepatite/parasitologia , Isquemia/imunologia , Isquemia/parasitologia , Leucócitos/efeitos da radiação , Leucopenia/etiologia , Fígado/imunologia , Fígado/parasitologia , Abscesso Hepático Amebiano/imunologia , Abscesso Hepático Amebiano/parasitologia , Abscesso Hepático Amebiano/patologia , Masculino , Lesões Experimentais por RadiaçãoRESUMO
The mechanisms of host resistance in hepatic amebiasis are poorly understood. Previous studies in guinea-pigs have shown that amebic liver infection is mild and cures spontaneously in approximately four days, in contrast to hamsters, where amebic liver infection progresses to coalescent abscesses that kill the animals in about one month. To determine the role of macrophages in the resistance of guinea-pigs to hepatic amebic infection, animals were treated with intraportal injection of Entamoeba histolytica, using the same route. Results showed that the amebic hepatic lesions are larger and require longer time to cure in the silica-treated group. This suggests that macrophages play a role in the resistance of the guinea-pig to amebic liver infection. The possible dependence of T lymphocytes in the resistance of guinea pigs to amebic hepatic infection was analyzed using Cyclosporin A. Results showed that resistance to E. histolytica liver infection is not related to circulating T lymphocytes. We conclude that the guinea-pig is a suitable experimental model for the study of natural host resistance mechanisms in hepatic amebiasis. Macrophages, but not T lymphocytes participate as an effective cellular immune response to eradicate amebic infection in the liver of guinea-pigs.