Host-derived annexin II at the host-parasite interface of the Echinococcus granulosus hydatid cyst.
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Amino Acid Sequence↗
Biomedical subjects
M Breijo
Publications and source records attributed to M Breijo.
How Echinococcus granulosus deals with complement.
Here, Ana Mar a 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.
Animals↗
Contribution of C5-mediated mechanisms to host defence against Echinococcus granulosus hydatid infection.
The aim of this work was to investigate the contribution of complement C5-mediated mechanisms, with an emphasis on inflammation, to host defences against Echinococcus granulosus hydatid disease. Thus, we compared the systemic and local inflammatory responses induced by the parasite, and the outcome of infection, between congenic C5-sufficient (B10.D2 n/SnJ) and C5-deficient (B10.D2 o/SnJ) mice challenged with protoscoleces. Indirect evidence of in-vivo complement activation during the establishment phase was obtained; infection induced serum amyloid P and eosinophil responses which were dependent on C5. Early recruitment of polymorphonuclear cells was not dependent on the presence of C5. The higher capacity of C5-sufficient mice to recruit eosinophils was also observed during the cystic phase of infection, and mice recruiting more eosinophils developed lower parasite masses. Analysis of the outcome of infection after 8 months showed that C5-sufficient mice were more resistant to infection than C5-deficient mice in terms of individuals with no cysts; this trend was not statistically significant. In addition, C5-deficient mice developed higher numbers of large (> 5 mm in diameter) cysts and higher cyst weights than C5-sufficient mice indicating that C5-mediated mechanisms are detrimental for parasite growth. Taken together, our results suggest that complement, through C5-mediated effectors, contributes to host defences by both restricting the establishment of infection and controlling the growth of established cysts. This contribution may, at least partially, be associated with the ability of C5a to promote eosinophil infiltration.
Animals↗
The 14-3-3 protein is secreted by the adult worm of Echinococcus granulosus.
The 14-3-3 protein, already described in the metacestode of Echinococcus multilocularis, has been characterized in the Echinococcus granulosus adult worm. Immunolocalization studies show the presence of the 14-3-3 protein in the periphery of testes and externally associated with the apical rostellum and adjacent worm tegument. The alcian blue staining in consecutive parasite sections gave similar reactivity patterns, suggesting that the 14-3-3 protein is produced and secreted by rostellar glands. Immunoblot analysis showed the presence of the 14-3-3 protein in somatic and excretory-secretory worm products with higher and smaller apparent molecular masses, respectively, than those detected in E. multilocularis or E. granulosus metacestode tissues. Conversely, the 14-3-3 protein was not detected in metacestode secretory products. Detection of anti-E. granulosus 14-3-3 reactivity in sera of experimentally infected dogs was achieved at early stages of infection. Specific antibody titres decreased during the course of infection. The possible origin and functions of the 14-3-3 protein produced by the adult worm are discussed.
14-3-3 Proteins↗
Echinococcus granulosus: an intraperitoneal diffusion chamber model of secondary infection in mice.
The present work describes a new experimental model of secondary infection which allows, through the recovery of the parasite together with its local in vivo environment, examination of the local nonadaptive immune response of the infected host and the differentiation of the parasite from protoscoleces to cysts. In this model we administered protoscoleces within silicone diffusion chambers, previously implanted into the peritoneal cavities of mice. The process of designing the model involved, first, determination of the optimal time postimplantation to infect the mice and, second, evaluation of the parasite's ability to establish infection within the chambers. The optimal time for infection was considered to be after the inflammation caused by implantation of the chambers had subsided. Our results showed that by day 20 postsurgery, three parameters used as indications of inflammation (complement C3, serum amyloid P protein, and polymorphonuclear cells in the peritoneum and in the chamber contents) had reverted to their normal levels. In our study of parasite differentiation, we found that 2-3% of the total number of parasites inoculated into the chambers were recovered as viable cysts after 100 days. Throughout the infection period, the population of parasites recovered was heterogeneous; certain parasite morphologies that have not been described previously were observed. In conclusion, the use of intraperitoneal diffusion chambers offers a potential tool for investigating the in vivo differentiation process of secondary cysts of Echinococcus granulosus in mice and the early local interactions between host and parasite during this process.
Animals↗