Echinococcus granulosus: The establishment of the metacestode is associated with control of complement-mediated early inflammation

• Published in: Experimental parasitology 2008-02, Vol.118 (2), p.188-196
• Main Authors: Breijo, Martin, Anesetti, Gabriel, Martínez, Laura, Sim, Robert B., Ferreira, Ana M.
• Format: Article
• Language: English
• Subjects: animal disease models; Animals; Biological and medical sciences; biological development; Cattle; Cestode; cobra venom factor; complement; Complement activation; Complement Activation - physiology; complement C3; Complement C3 - analysis; Complement C3 - immunology; complement component C3; CVF; D/I; day post-infection; decomplemented infected mice; Diffusion Chambers, Culture; Disease Models, Animal; Down-Regulation; dpi; E. granulosus; echinococcosis; Echinococcosis - immunology; Echinococcosis - parasitology; Echinococcosis - pathology; Echinococcus granulosus; Echinococcus granulosus - growth & development; Echinococcus granulosus - immunology; Female; Fundamental and applied biological sciences. Psychology; HCW; Hydatid cyst; hydatid cyst wall; hydatids; IgG; IgM; immunoglobulin G; Immunoglobulin G - metabolism; immunoglobulin M; Immunoglobulin M - metabolism; Immunohistochemistry; infection; Inflammation; Inflammation - immunology; Inflammation - parasitology; Inflammation - pathology; inflammatory reaction; intraperitoneal; Life cycle. Host-agent relationship. Pathogenesis; metacestodes; Mice; Mice, Inbred BALB C; mortality; N/I; normocomplementemic infected mice; PBS; PBS containing 0.05% Tween 20; PBS-T; phosphate buffered saline; protoscoleces; Protozoa; PSC; TCC; terminal complement complex
• ISSN: 0014-4894; 1090-2449
• DOI: 10.1016/j.exppara.2007.07.014

In this work we studied the evolution of early inflammation, complement activation and parasite survival/death along the establishment phase of Echinococcus granulosus metacestode. Using a chamber model of infection in mice, we examined cell infiltration and C3 deposition on individual parasites during their development from protoscoleces to cystic forms. We found that the intensity of the initial inflammation decreased around undamaged but not around damaged parasites: at 43 dpi undamaged parasites were mostly associated with poor/mild inflammation while damaged parasites with a strong inflammation. In addition, whereas complement activation participated in the induction of early inflammation, the deposition of C3 on undamaged parasites progressively diminished. Interestingly, we observed some parasites in pre-cystic stage with no/poor C3 deposition at 3 dpi. Overall, these results indicated that the establishment and survival of the hydatid cyst is associated with the control of complement and, consequently, of local inflammation at the initial phases of infection.