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诱导型一氧化氮合酶缺陷小鼠中莱姆关节炎的发展

Development of lyme arthritis in mice deficient in inducible nitric oxide synthase.

作者信息

Brown C R, Reiner S L

机构信息

Department of Medicine, University of Chicago, Chicago, IL 60637.

出版信息

J Infect Dis. 1999 Jun;179(6):1573-6. doi: 10.1086/314774.

DOI:10.1086/314774
PMID:10228086
Abstract

Nitric oxide (NO) is a powerful antimicrobial agent and an important regulatory molecule of the innate immune response. To determine if NO has a role in experimental Lyme disease, arthritis-resistant DBA/2J and arthritis-susceptible C3H/HeJ mice were bred to be genetically deficient for inducible NO synthase (iNOS). Following footpad injection of Borrelia burgdorferi, arthritis was similar between iNOS-deficient and control animals regardless of their genetic background. Histologic examination and arthritis severity scores of ankles revealed no differences in arthritis development between iNOS-deficient and control animals. Despite being deficient in a key antimicrobial agent, iNOS-deficient mice had tissue levels of B. burgdorferi similar to those in control mice. Thus, NO does not have a critical role in susceptibility to Lyme arthritis through tissue damage via an overexuberant inflammatory response, nor is it required in resistance through the clearance of spirochetes from tissues.

摘要

一氧化氮(NO)是一种强大的抗菌剂,也是先天性免疫反应的重要调节分子。为了确定NO在实验性莱姆病中是否起作用,将抗关节炎的DBA/2J小鼠和易患关节炎的C3H/HeJ小鼠培育成诱导型一氧化氮合酶(iNOS)基因缺陷型。在足垫注射伯氏疏螺旋体后,无论基因背景如何,iNOS缺陷型动物和对照动物的关节炎情况相似。对踝关节的组织学检查和关节炎严重程度评分显示,iNOS缺陷型动物和对照动物在关节炎发展方面没有差异。尽管缺乏一种关键的抗菌剂,但iNOS缺陷型小鼠体内伯氏疏螺旋体的组织水平与对照小鼠相似。因此,NO在通过过度炎症反应造成组织损伤而导致莱姆关节炎易感性方面没有关键作用,在通过从组织中清除螺旋体产生抗性方面也不是必需的。

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Development of lyme arthritis in mice deficient in inducible nitric oxide synthase.诱导型一氧化氮合酶缺陷小鼠中莱姆关节炎的发展
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