Susceptibility versus resistance in alveolar echinococcosis (larval infection with Echinococcus multilocularis).

Gottstein, Bruno; Wang, Junhua; Boubaker, Ghalia; Marinova, Irina; Spiliotis, Markus; Müller, Norbert; Hemphill, Andrew (2015). Susceptibility versus resistance in alveolar echinococcosis (larval infection with Echinococcus multilocularis). Veterinary parasitology, 213(3-4), pp. 103-109. Elsevier 10.1016/j.vetpar.2015.07.029

[img]
Preview
Text
1-s2.0-S0304401715003696-main.pdf - Published Version
Available under License Creative Commons: Attribution-Noncommercial-No Derivative Works (CC-BY-NC-ND).

Download (1MB) | Preview

Epidemiological studies have demonstrated that the majority of human individuals exposed to infection with Echinococcus spp. eggs exhibit resistance to disease as shown by either seroconversion to parasite--specific antigens, and/or the presence of 'dying out' or 'aborted' metacestodes, not including hereby those individuals who putatively got infected but did not seroconvert and who subsequently allowed no development of the pathogen. For those individuals where infection leads to disease, the developing parasite is partially controlled by host immunity. In infected humans, the type of immune response developed by the host accounts for the subsequent trichotomy concerning the parasite development: (i) seroconversion proving infection, but lack of any hepatic lesion indicating the failure of the parasite to establish and further develop within the liver; or resistance as shown by the presence of fully calcified lesions; (ii) controlled susceptibility as found in the "conventional" alveolar echinococcosis (AE) patients who experience clinical signs and symptoms approximately 5-15 years after infection, and (iii) uncontrolled hyperproliferation of the metacestode due to an impaired immune response (AIDS or other immunodeficiencies). Immunomodulation of host immunity toward anergy seems to be triggered by parasite metabolites. Beside immunomodulating IL-10, TGFβ-driven regulatory T cells have been shown to play a crucial role in the parasite-modulated progressive course of AE. A novel CD4+CD25+ Treg effector molecule FGL2 recently yielded new insight into the tolerance process in Echinococcus multilocularis infection.

Item Type:

Journal Article (Original Article)

Division/Institute:

05 Veterinary Medicine > Research Foci > Host-Pathogen Interaction
05 Veterinary Medicine > Department of Infectious Diseases and Pathobiology (DIP) > Institute of Parasitology
05 Veterinary Medicine > Department of Infectious Diseases and Pathobiology (DIP)

UniBE Contributor:

Gottstein, Bruno; Wang, Junhua; Boubaker, Ghalia; Marinova, Irina; Spiliotis, Markus; Müller, Norbert and Hemphill, Andrew

Subjects:

600 Technology > 630 Agriculture

ISSN:

0304-4017

Publisher:

Elsevier

Language:

English

Submitter:

Bruno Gottstein

Date Deposited:

25 May 2016 11:34

Last Modified:

31 Oct 2018 10:36

Publisher DOI:

10.1016/j.vetpar.2015.07.029

PubMed ID:

26260407

Uncontrolled Keywords:

Alveolar echinococcosis, Em18-ELISA, FGL2, PET-CT, Regulatory T cells, Resistance, Susceptibility, TGF-beta

BORIS DOI:

10.7892/boris.82010

URI:

https://boris.unibe.ch/id/eprint/82010

Actions (login required)

Edit item Edit item
Provide Feedback