Abstract
Amoebiasis is a parasitic disease caused by Entamoeba histolytica. This illness is prevalent in poor countries causing 100,000 deaths worldwide. Knowledge of the natural resistance mechanisms of rats to amoebic liver abscess (ALA) development may help to discover new pathogenic factors and to design novel therapeutic strategies against amoebiasis. In this work, histologic analyses suggested that the complement system may play a central role in rat natural resistance to ALA. E. histolytica trophozoites disappeared from rat liver within 6 h post-infection with minimal or no inflammatory infiltrate. In vitro findings indicate that rat complement was lethal for the parasite. Furthermore, hamsters became resistant to ALA by intravenous administration of fresh rat serum before infection. The amoebicidal potency of rat complement was 10 times higher than hamster complement and was not related to their respective CH50 levels. The alternative pathway of complement plays a central role in its toxicity to E. histolytica since trypan blue, which is a C3b receptor inhibitor, blocks its amoebicidal activity. These results suggest that amoebic membrane affinity, high for C3b and/or low for Factor H, in comparison with the hamster ones, may result in higher deposition of membrane complex attack on parasite surface and death.
Highlights
Entamoeba histolytica is the protozoan parasite responsible for human amoebiasis that causes approximately 100,000 deaths each year worldwide [1]
Human complement activation by classical and alternative pathways has been observed in E. histolytica [19,20]
The alternative pathway or mannose-complement pathways involved in the amoebicidal sera effect could not be ruled out since the CH50 assays used in this work detect only the classical pathway [9,10] and species-specific recognition by the alternative pathway of complement has been documented [21]
Summary
Entamoeba histolytica is the protozoan parasite responsible for human amoebiasis that causes approximately 100,000 deaths each year worldwide [1]. It is an exclusive human disease and the parasite life cycle has not been reproduced in laboratory animals. Some mouse strains are partially susceptible to acute EALA, in which tissue damage is repaired after parasite elimination observed from 3 to 7 days [2]. Rats are totally resistant to EALA [3]. Knowledge of the natural resistance mechanisms to EALA in rats may allow to stimulate a specific response in susceptible animals that could lead to new therapeutic strategies for human amoebiasis
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