Development of Lyme arthritis in mice deficient in inducible nitric oxide synthase

被引:15
作者
Brown, CR
Reiner, SL
机构
[1] Univ Chicago, Gwen Knapp Ctr Lupus & Immunol Res, Comm Dev Biol, Comm Immunol, Chicago, IL 60637 USA
[2] Univ Chicago, Dept Med, Chicago, IL 60637 USA
关键词
D O I
10.1086/314774
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:1573 / 1576
页数:4
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