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How Echinococcus granulosus Deals with Complement

https://doi.org/10.1016/S0169-4758(99)01625-7Get rights and content

Abstract

Here, Ana Marı́a Ferreira and colleagues discuss the interplay between the larval stages of Echinococcus granulosus and an important effector arm of immunity: the host complement system. During early infection, the parasite activates complement, and hence complement-dependent inflammatory responses. However, on differentiation into the hydatid cyst, the parasite exposes to the host a structure – the cyst wall – that does not activate complement strongly. Mechanisms inhibiting complement activation on the cyst wall have been elucidated, contributing to the understanding of how this large, persistent, tissue-dwelling pathogen controls the inflammatory response.

Section snippets

The establishment phase

The infective stages of E. granulosus are susceptible in vitro to complement-mediated lysis, being killed by incubation in normal serum but not in heat-decomplemented serum, from a range of host species3, 4, 5, 6, 7. For oncospheres, the activation pathways of complement involved in parasite lysis have not been elucidated; however, the rate of killing is greatly enhanced by the presence of antibodies, reflecting the efficacy of classical pathway-driven activation7. Lysis of protoscoleces (PSCs)

The established cyst

An early and consistent observation of researchers studying interactions between E. granulosus and complement was the fact that hydatid cyst fluid contains molecules that trigger complement in vitro, mainly through the alternative pathway11, 12, 13. This activation is mostly the result of very high molecular weight carbohydrate-rich species present in cyst fluid14, 15. We think that the biological significance of this activation is not straightforward, as cyst fluid is not normally in contact

Conclusion

The precystic stages of E. granulosus trigger the important innate recognition mechanism represented by the alternative pathway of complement. This activation contributes to the host inflammatory response and, in particular, to the recruitment of eosinophils. Upon differentiation to the cystic form, the parasite exposes an outer structure that seems not to trigger complement, either through innate or adaptive pathways. Inhibitory mechanisms must account for this avoidance, and some of these are

Acknowledgements

This work was supported by the European Commission’s DGXIIB ISC programme, CONICYT (Ministry of Education, Uruguay), The Wellcome Trust, CSIC (University of Uruguay) and PEDECIBA (Uruguay). We thank Berta Burghi for help with figures.

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