Parasite-Specific IL-17-Type Cytokine Responses and Soluble IL-17 Receptor Levels in Alveolar Echinococcosis Patients

Author:

Lechner Christian J.1,Grüner Beate2,Huang Xiangsheng1,Hoffmann Wolfgang H.1,Kern Peter2,Soboslay Peter T.1

Affiliation:

1. Institute for Tropical Medicine, University of Tübingen Clinics, 72074 Tübingen, Germany

2. Division of Infectious Diseases and Clinical Immunology, Comprehensive Infectious Disease Center, University of Ulm Hospitals, 89081 Ulm, Germany

Abstract

Alveolar Echinococcosis (AE) caused by the cestodeEchinococcus multilocularis, is a severe helminth infection of man, where unrestricted parasite growth will ultimately result in organ failure and fatality. The tissue-infiltrative growth of the larval metacestode and the limited efficacy of available drugs complicate successful intervention in AE; patients often need life-long medication, and if possible, surgical resection of affected tissues and organs. Resistance to AE has been reported, but the determinants which confer protection are not known. ln this study, we analyzed in patients at distinct stages of Alveolar Echirococcosis, that is cured, stable and progressive AE, as well as in infection-free controls, the cellular production and plasma levels of pro-inflammatory cytokines lL-17A, lL-17B, lL-17F and their soluble receptors lL-17RA (slL-17RA) and IL-17RB (sIL-17RB). Significantly elevated levels of IL-17B and slL-17RB were observed, whilst lL-17F and slL-17RA were reduced in patients with AE. Similarly, the cellular production of lL-17F and slL-L7RA in response toE. multilocularisantigens was low in AE patients, while levels of slL-17RB were highly enhanced. These observations suggest immune-modulating properties ofE. multitocularison lL-17 cytokine-mediated pro-inflammatory immune responses; this may facilitate the tissue infiltrative growth of the parasite and its persistence in the human host.

Funder

Baden-Württemberg Stiftung

Publisher

Hindawi Limited

Subject

General Medicine,Immunology,Immunology and Allergy

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