Parasite-specific IL-17-type cytokine responses and soluble IL-17 receptor levels in Alveolar Echinococcosis patients

Christian J. Lechner, Beate Grüner, Xiangsheng Huang, Wolfgang H. Hoffmann, Peter Kern, Peter T. Soboslay

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Alveolar Echinococcosis (AE) caused by the cestode Echinococcus 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 to E. multilocularis antigens was low in AE patients, while levels of slL-17RB were highly enhanced. These observations suggest immune-modulating properties of E. multitocularis on 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.

Original languageEnglish (US)
Article number735342
JournalClinical and Developmental Immunology
Volume2012
DOIs
StatePublished - 2012
Externally publishedYes

Fingerprint

Interleukin-17 Receptors
Interleukin-17
Parasites
Cytokines
Echinococcus multilocularis
Growth
Cestoda
Helminths
Infection Control
Alveolar echinococcosis
Antigens
Infection

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Medicine(all)

Cite this

Parasite-specific IL-17-type cytokine responses and soluble IL-17 receptor levels in Alveolar Echinococcosis patients. / Lechner, Christian J.; Grüner, Beate; Huang, Xiangsheng; Hoffmann, Wolfgang H.; Kern, Peter; Soboslay, Peter T.

In: Clinical and Developmental Immunology, Vol. 2012, 735342, 2012.

Research output: Contribution to journalArticle

Lechner, Christian J. ; Grüner, Beate ; Huang, Xiangsheng ; Hoffmann, Wolfgang H. ; Kern, Peter ; Soboslay, Peter T. / Parasite-specific IL-17-type cytokine responses and soluble IL-17 receptor levels in Alveolar Echinococcosis patients. In: Clinical and Developmental Immunology. 2012 ; Vol. 2012.
@article{834b5b3f9288499b9277e9011408082e,
title = "Parasite-specific IL-17-type cytokine responses and soluble IL-17 receptor levels in Alveolar Echinococcosis patients",
abstract = "Alveolar Echinococcosis (AE) caused by the cestode Echinococcus 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 to E. multilocularis antigens was low in AE patients, while levels of slL-17RB were highly enhanced. These observations suggest immune-modulating properties of E. multitocularis on 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.",
author = "Lechner, {Christian J.} and Beate Gr{\"u}ner and Xiangsheng Huang and Hoffmann, {Wolfgang H.} and Peter Kern and Soboslay, {Peter T.}",
year = "2012",
doi = "10.1155/2012/735342",
language = "English (US)",
volume = "2012",
journal = "Journal of Immunology Research",
issn = "2314-8861",
publisher = "Hindawi Publishing Corporation",

}

TY - JOUR

T1 - Parasite-specific IL-17-type cytokine responses and soluble IL-17 receptor levels in Alveolar Echinococcosis patients

AU - Lechner, Christian J.

AU - Grüner, Beate

AU - Huang, Xiangsheng

AU - Hoffmann, Wolfgang H.

AU - Kern, Peter

AU - Soboslay, Peter T.

PY - 2012

Y1 - 2012

N2 - Alveolar Echinococcosis (AE) caused by the cestode Echinococcus 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 to E. multilocularis antigens was low in AE patients, while levels of slL-17RB were highly enhanced. These observations suggest immune-modulating properties of E. multitocularis on 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.

AB - Alveolar Echinococcosis (AE) caused by the cestode Echinococcus 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 to E. multilocularis antigens was low in AE patients, while levels of slL-17RB were highly enhanced. These observations suggest immune-modulating properties of E. multitocularis on 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.

UR - http://www.scopus.com/inward/record.url?scp=84867028284&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84867028284&partnerID=8YFLogxK

U2 - 10.1155/2012/735342

DO - 10.1155/2012/735342

M3 - Article

C2 - 22969818

AN - SCOPUS:84867028284

VL - 2012

JO - Journal of Immunology Research

JF - Journal of Immunology Research

SN - 2314-8861

M1 - 735342

ER -