RESUMO
We examined the participation of polymorphonuclear leucocytes and amebic proteinases upon tissue damage by means of an experimental model of acute amebic lesions developed in rat's testicle. In leukopenic rats (less than 1,000 leucocytes/ml) intratesticular injection of axenic E. histolytica's trophozoites (HM-1) produced lesions undistinguishable from the normal controls. On the other hand, inhibition of 80% (average) of the proteinase activity by means of previous incubation of the trophozoites with human a2M gave way to minimal inflammatory lesions almost undistinguishable from the controls which were injected with PBS-A. Our data suggest that in this experimental model of acute amebiasis polymorphonuclear leukocytes do not participate in the tissue damage and that amebic proteinases are responsible for Entamoeba histolytica's virulence.
Assuntos
Endopeptidases/fisiologia , Entamoeba histolytica/patogenicidade , Entamebíase/patologia , Neutrófilos/fisiologia , Orquite/parasitologia , Proteínas de Protozoários/metabolismo , Animais , Entamoeba histolytica/enzimologia , Entamebíase/complicações , Entamebíase/enzimologia , Leucopenia/induzido quimicamente , Leucopenia/complicações , Masculino , Mecloretamina/toxicidade , Necrose , Orquite/complicações , Orquite/patologia , Inibidores de Proteases/farmacologia , Ratos , Ratos Endogâmicos , Virulência , alfa-Macroglobulinas/farmacologiaRESUMO
Even though eosinophiles are not characteristic of amebiasis, polymorphonuclear eosinophilic cells are regularly found in the inflammatory lesion which occurs in the early phases of amebic invasion. To acquire better knowledge of the intervention of these cells when confronted with E. histolytica, testicular lesions were produced by means of direct injection of amebas in rats with eosinophilia. Eosinophilia (greater than or equal to 4%) was induced in male Sprague Dawley rats by an intravenous injection of Sephadex G200 suspension. Later, both the eosinophilic and normal (control) rats were challenged with an intratesticular injection (on the left side) of 2 x 10(6) amebas of the virulent strain HM1-IMSS. The other testicle was injected with BFS-A to serve as control. The testicles were removed 5 hours later and evaluated histologically. The size and celullarity of the testicular lesions produced by the ameba on both eosinophilic and controls were similar, whereas lesions were not found in testicles injected with BSF-A. Within the limits of our experimental model, the results suggest that eosinophils do not contribute substantially to the genesis of tissue lesions produced by E. histolytica.