文章基本信息

标题：The neuropathic phenotype of the K/BxN transgenic mouse with spontaneous arthritis: pain, nerve sprouting and joint remodeling
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作者：Gilson Gonçalves dos Santos ; Juan Miguel Jimenéz-Andrade ; Sarah A. Woller 等
期刊名称：Scientific Reports
电子版ISSN：2045-2322
出版年度：2020
卷号：10
期号：1
页码：1-12
DOI：10.1038/s41598-020-72441-5
出版社：Springer Nature
摘要：The adult K/BxN transgenic mouse develops spontaneous autoimmune arthritis with joint remodeling and profound bone loss. We report that both males and females display a severe sustained tactile allodynia which is reduced by gabapentin but not the potent cyclooxygenase inhibitor ketorolac. In dorsal horn, males and females show increased GFAP astrocytic cells; however, only males demonstrate an increase in Iba1 microglia. In dorsal root ganglia (DRG), there is an increase in CGRP , TH , and Iba1 (macrophage) labeling, but no increase in ATF3 cells. At the ankle there is increased CGRP , TH , and GAP-43 fiber synovial innervation. Thus, based on the changes in dorsal horn, DRG and peripheral innervation, we suggest that the adult K/BxN transgenic arthritic mice display a neuropathic phenotype, an assertion consistent with the analgesic pharmacology seen in this animal. These results indicate the relevance of this model to our understanding of the nociceptive processing which underlies the chronic pain state that evolves secondary to persistent joint inflammation.
其他摘要：Abstract The adult K/BxN transgenic mouse develops spontaneous autoimmune arthritis with joint remodeling and profound bone loss. We report that both males and females display a severe sustained tactile allodynia which is reduced by gabapentin but not the potent cyclooxygenase inhibitor ketorolac. In dorsal horn, males and females show increased GFAP astrocytic cells; however, only males demonstrate an increase in Iba1 microglia. In dorsal root ganglia (DRG), there is an increase in CGRP , TH , and Iba1 (macrophage) labeling, but no increase in ATF3 cells. At the ankle there is increased CGRP , TH , and GAP-43 fiber synovial innervation. Thus, based on the changes in dorsal horn, DRG and peripheral innervation, we suggest that the adult K/BxN transgenic arthritic mice display a neuropathic phenotype, an assertion consistent with the analgesic pharmacology seen in this animal. These results indicate the relevance of this model to our understanding of the nociceptive processing which underlies the chronic pain state that evolves secondary to persistent joint inflammation.