Interferon‐α curbs production of interleukin‐22 by human peripheral blood mononuclear cells exposed to live Borrelia burgdorferi

Journal of Cellular and Molecular Medicine

Anika Berner²  Malte Bachmann²  Josef Pfeilschifter²  Peter Kraiczy¹ 

[1] Institute of Medical Microbiology and Infection Control, University Hospital Goethe-University Frankfurt, Frankfurt am Main, Germany;Pharmazentrum Frankfurt/ZAFES, University Hospital Goethe-University Frankfurt, Frankfurt am Main, Germany

关键词: interleukin‐1;    interleukin‐22;    interferon‐α;    inflammation;    host defence;    immune response;    Borrelia burgdorferi;    peripheral blood mononuclear cells;   

DOI  :  10.1111/jcmm.12634

来源: Wiley

【 摘 要 】

Abstract

Cytokine networks initiated by means of innate immunity are regarded as a major determinant of host defence in response to acute infection by bacteria including Borrelia burgdorferi. Herein, we demonstrate that interferon (IFN)-α, either endogenously produced after exposure of cells to toll-like receptor-9-activating CpG oligonucleotides or provided as recombinant cytokine, weakens activation of the anti-bacterial interleukin (IL)-1/IL-22 axis in human peripheral blood mononuclear cells exposed to viable B. burgdorferi. As IFN-α has been related to pathological dissemination of the spirochaete, data suggest an immunoregulatory role of type I IFN in this context that is able to significantly modify cytokine profiles thereby possibly determining early course of B. burgdorferi infection.

【 授权许可】

CC BY   
© 2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

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