Abstract
BackgroundCystic echinococcosis is a worldwide distributed helminth zoonosis caused by the larval stage of Echinococcus granulosus. Human secondary cystic echinococcosis is caused by dissemination of protoscoleces after accidental rupture of fertile cysts and is due to protoscoleces ability to develop into new metacestodes. In the experimental model of secondary cystic echinococcosis mice react against protoscoleces producing inefficient immune responses, allowing parasites to develop into cysts. Although the chronic phase of infection has been analyzed in depth, early immune responses at the site of infection establishment, e.g., peritoneal cavity, have not been well studied. Because during early stages of infection parasites are thought to be more susceptible to immune attack, this work focused on the study of cellular and molecular events triggered early in the peritoneal cavity of infected mice.Principal FindingsData obtained showed disparate behaviors among subpopulations within the peritoneal lymphoid compartment. Regarding B cells, there is an active molecular process of plasma cell differentiation accompanied by significant local production of specific IgM and IgG2b antibodies. In addition, peritoneal NK cells showed a rapid increase with a significant percentage of activated cells. Peritoneal T cells showed a substantial increase, with predominance in CD4+ T lymphocytes. There was also a local increase in Treg cells. Finally, cytokine response showed local biphasic kinetics: an early predominant induction of Th1-type cytokines (IFN-γ, IL-2 and IL-15), followed by a shift toward a Th2-type profile (IL-4, IL-5, IL-6, IL-10 and IL-13).ConclusionsResults reported here open new ways to investigate the involvement of immune effectors players in E. granulosus establishment, and also in the sequential promotion of Th1- toward Th2-type responses in experimental secondary cystic echinococcosis. These data would be relevant for designing rational therapies based on stimulation of effective responses and blockade of evasion mechanisms.
Highlights
Helminths are metazoan parasites currently infecting a quarter of the world population [1]
Results reported here open new ways to investigate the involvement of immune effectors players in E. granulosus establishment, and in the sequential promotion of Th1- toward Th2-type responses in experimental secondary cystic echinococcosis
During infection establishment parasites are more susceptible to immune attack, our study focused on the immunological phenomena triggered early in the peritoneal cavity of experimentally infected mice
Summary
Helminths are metazoan parasites currently infecting a quarter of the world population [1]. The high prevalence of helminthiasis reflects one outstanding feature of parasite infections: chronicity. This fact could be read into helminths having special skills to adapt to defense mechanisms triggered by infected hosts, in order to survive for long periods of time. Chronicity observed in the context of parasite infections often associates with polarized cytokine responses. In the experimental model of secondary cystic echinococcosis mice react against protoscoleces producing inefficient immune responses, allowing parasites to develop into cysts. Because during early stages of infection parasites are thought to be more susceptible to immune attack, this work focused on the study of cellular and molecular events triggered early in the peritoneal cavity of infected mice
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