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用伯氏疏螺旋体感染白细胞介素17受体A缺陷的C3H小鼠,并不影响它们莱姆关节炎和心肌炎的发展。

Infection of Interleukin 17 Receptor A-Deficient C3H Mice with Borrelia burgdorferi Does Not Affect Their Development of Lyme Arthritis and Carditis.

作者信息

Lasky Carrie E, Jamison Kara E, Sidelinger Darcie R, Pratt Carmela L, Zhang Guoquan, Brown Charles R

机构信息

Department of Veterinary Pathobiology, University of Missouri, Columbia, Missouri, USA.

Department of Veterinary Pathobiology, University of Missouri, Columbia, Missouri, USA

出版信息

Infect Immun. 2015 Jul;83(7):2882-8. doi: 10.1128/IAI.00533-15. Epub 2015 May 4.

DOI:10.1128/IAI.00533-15
PMID:25939508
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4468557/
Abstract

Recently, a number of studies have reported the presence of interleukin 17 (IL-17) in patients with Lyme disease, and several murine studies have suggested a role for this cytokine in the development of Lyme arthritis. However, the role of IL-17 has not been studied using the experimental Lyme borreliosis model of infection of C3H mice with Borrelia burgdorferi. In the current study, we investigated the role of IL-17 in the development of experimental Lyme borreliosis by infecting C3H mice devoid of the common IL-17 receptor A subunit (IL-17RA) and thus deficient in most IL-17 signaling. Infection of both C3H and C3H IL-17RA(-/-) mice led to the production of high levels of IL-17 in the serum, low levels in the heart tissue, and no detectable IL-17 in the joint tissue. The development and severity of arthritis and carditis in the C3H IL-17RA(-/-) mice were similar to what was seen in wild-type C3H mice. In addition, development of antiborrelia antibodies and clearance of spirochetes from tissues were similar for the two mouse strains. These results demonstrate a limited role for IL-17 signaling through IL-17RA in the development of disease following infection of C3H mice with B. burgdorferi.

摘要

最近,多项研究报告了莱姆病患者体内存在白细胞介素17(IL-17),并且一些小鼠研究表明这种细胞因子在莱姆关节炎的发展中起作用。然而,尚未使用伯氏疏螺旋体感染C3H小鼠的实验性莱姆病螺旋体病模型来研究IL-17的作用。在当前研究中,我们通过感染缺乏常见IL-17受体A亚基(IL-17RA)从而在大多数IL-17信号传导方面存在缺陷的C3H小鼠,研究了IL-17在实验性莱姆病螺旋体病发展中的作用。C3H和C3H IL-17RA(-/-)小鼠的感染均导致血清中产生高水平的IL-17,心脏组织中产生低水平的IL-17,而关节组织中未检测到IL-17。C3H IL-17RA(-/-)小鼠中关节炎和心肌炎的发展及严重程度与野生型C3H小鼠相似。此外,两种小鼠品系的抗伯氏疏螺旋体抗体的产生以及组织中螺旋体的清除情况相似。这些结果表明,通过IL-17RA的IL-17信号传导在伯氏疏螺旋体感染C3H小鼠后疾病的发展中作用有限。

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