Guillain Barré Syndrome is induced in Non-Obese Diabetic (NOD) mice following Campylobacter jejuni infection and is exacerbated by antibiotics

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• 作者：J.L. St Charles^a ; ^b ; ^d ; J.A. Bell^a ; ^d ; B.J. Gadsden^a ; ^b ; ^d ; A. Malik^a ; ^c ; ^d ; H. Cooke^d ; L.K. Van de Grift^d ; H.Y. Kim^a ; E.J. Smith^a ; ^d ; L.S. Mansfield^a ; ^c ; ^d ; ^{mansfie4@cvm.msu.edu}
• 关键词：Campylobacter jejuni ; Guillain Barré ; Syndrome ; Peripheral neuropathy ; Autoimmunity ; Mouse models
• 刊名：Journal of Autoimmunity
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：77
• 期：Complete
• 页码：11-38
• 全文大小：8087 K
• 卷排序：77

文摘

We showed that GBS is induced in NOD mice following Campylobacter jejuni infection and is exacerbated by antibiotics. C. jejuni strain genotype, host genotype and antibiotic treatment affected GBS disease outcomes and many disease phenotypes were possible. These mouse models of GBS can be judged for robustness after infection with C. jejuni strains based on evaluation of three factors—onset of GBS clinical signs/phenotypes, anti-ganglioside autoantibodies and nerve lesions. Because GBS produces segmental neurological lesions, we improved assessments of nerves by dissecting the entire sciatic nerve, dorsal nerve root and brachial plexus, which were embedded en bloc. These mouse models show promise for studying underlying mechanisms of GBS and for developing new therapeutics or preventatives.