Research Progress on the Animal Models of Neuromyelitis Optica Spectrum Disorders-related Neuropathic Pain
-
摘要:
视神经脊髓炎谱系疾病(neuromyelitis optica spectrum disorders, NMOSD)是一种中枢神经系统炎性脱髓鞘性疾病,临床特征包括视神经炎,纵向长节段脊髓炎,及其引起的神经病理性疼痛。 受限于动物模型的缺乏,目前NMOSD神经病理性疼痛机制尚不明确,尽管已有部分研究证实神经病理性疼痛在NMOSD动物模型中的存在,但这些模型尚不成熟,未来亟需建立可靠且简便易行的NMOSD神经病理性疼痛动物模型,以帮助阐明发病机制,挖掘更有效的治疗手段。 本文对NMOSD相关神经病理性疼痛动物模型的研究进展进行综述,并对理想的动物模型及未来发展方向进行展望。
-
关键词:
- 视神经脊髓炎谱系疾病 /
- 脱髓鞘疾病 /
- 神经病理性疼痛 /
- 动物模型
Abstract:Neuromyelitis optica spectrum disorder (NMOSD) is an inflammatory demyelinating disease of central nervous system, characterized by optic neuritis and longitudinally extensive transverse myelitis, together with neuropathic pain. Limited by the lack of mature animal models, the mechanism of neuropathic pain in NMOSD is still unclear. Although some studies have reported neuropathic pain in NMOSD models, it is necessary to build a reliable and feasible animal model of NMOSD related neuropathic pain, which could provide scientific support for the mechanism and he mining of therapeutic targets. This article reviews research progress on the animal models of NMOSD related neuropathic pain. The prospects of ideal animal models and development tendencies are also described.
-
[1] WINGERCHUK D M, BANWELL B, BENNETT J L, et al. International consensus diagnostic criteria for neuromyelitis optica spectrum disorders[J]. Neurology, 2015, 85(2):177-89. [2] LUCCHINETTI C F, GUO Y, POPESCU B F G, et al. The pathology of an autoimmune astrocytopathy:lessons learned from neuromyelitis optica[J]. Brain Pathol, 2014, 24(1):83-97. [3] ASSEYER S, COOPER G, PAUL F. Pain in NMOSD and MOGAD:A Systematic Literature Review of Pathophysiology, Symptoms, and Current Treatment Strategies[J]. Front Neurol, 2020, 11(778. [4] AYZENBERG I, RICHTER D, HENKE E, et al. Pain, Depression, and Quality of Life in Neuromyelitis Optica Spectrum Disorder:A Cross-Sectional Study of 166 AQP4 AntibodySeropositive Patients[J]. Neurol Neuroimmunol Neuroinflamm, 2021, 8(3): [5] KANAMORI Y, NAKASHIMA I, TAKAI Y, et al. Pain in neuromyelitis optica and its effect on quality of life:a cross-sectional study[J]. Neurology, 2011, 77(7):652-8. [6] QIAN P, LANCIA S, ALVAREZ E, et al. Association of neuromyelitis optica with severe and intractable pain[J]. Arch Neurol, 2012, 69(11):1482-7. [7] ZHAO S, MUTCH K, ELSONE L, et al. Neuropathic pain in neuromyelitis optica affects activities of daily living and quality of life[J]. Mult Scler, 2014, 20(12):1658-61. [8] ZHANG X, XU Y, PEI L-J. Review of Neuromyelitis Optica Spectrum Disorder with PainDepression Comorbidity[J]. Chin Med Sci J, 2021, 36(4):316-22. [9] ASSEYER S, COOPER G, PAUL F. Pain in NMOSD and MOGAD:A Systematic Literature Review of Pathophysiology, Symptoms, and Current Treatment Strategies[J]. Front Neurol, 2020, 11(778. [10] ZHANG X, PEI L, XU Y, et al. Factors correlated with neuropathic pain in patients with neuromyelitis optica spectrum disorder[J]. Mult Scler Relat Disord, 2022, 68(104213. [11] LI X, XU H, ZHENG Z, et al. The risk factors of neuropathic pain in neuromyelitis optica spectrum disorder:a retrospective case-cohort study[J]. BMC Neurology, 2022, 22(1):304. [12] GRACE P M, LORAM L C, CHRISTIANSON J P, et al. Behavioral assessment of neuropathic pain, fatigue, and anxiety in experimental autoimmune encephalomyelitis (EAE) and attenuation by interleukin-10 gene therapy[J]. Brain Behav Immun, 2017, 59(49-54. [13] KHAN N, WOODRUFF T M, SMITH M T. Establishment and characterization of an optimized mouse model of multiple sclerosis-induced neuropathic pain using behavioral, pharmacologic, histologic and immunohistochemical methods[J]. Pharmacol Biochem Behav, 2014, 126(13-27. [14] KWILASZ A J, GREEN FULGHAM S M, DURAN-MALLE J C, et al. Toll-like receptor 2 and 4 antagonism for the treatment of experimental autoimmune encephalomyelitis (EAE)-related pain[J]. Brain Behav Immun, 2021, 93(80-95. [15] IWAMOTO S, ITOKAZU T, SASAKI A, et al. RGMa Signal in Macrophages Induces Neutrophil-Related Astrocytopathy in NMO[J]. Ann Neurol, 2022, 91(4):532-47. [16] KUROSAWA K, MISU T, TAKAI Y, et al. Severely exacerbated neuromyelitis optica rat model with extensive astrocytopathy by high affinity anti-aquaporin-4 monoclonal antibody[J]. Acta Neuropathologica Communications, 2015, 3(82. [17] HILLEBRAND S, SCHANDA K, NIGRITINOU M, et al. Circulating AQP4-specific aoantibodies alone can induce neuromyelitis optica spectrum disorder in the rat[J]. Acta Neuropathol, 2019, 137(3):467-85. [18] CHAN K H, ZHANG R, KWAN J S C, et al. Aquaporin-4 autoantibodies cause asymptomatic aquaporin-4 loss and activate astrocytes in mouse[J]. J Neuroimmunol, 2012, 245(1-2):32-8. [19] KINOSHITA M, NAKATSUJI Y, KIMURA T, et al. Neuromyelitis optica:Passive transfer to rats by human immunoglobulin[J]. Biochem Biophys Res Commun, 2009, 386(4):623-7. [20] SAINI H, RIFKIN R, GORELIK M, et al. Passively transferred human NMO-IgG exacerbates demyelination in mouse experimental autoimmune encephalomyelitis[J]. BMC Neurology, 2013, 13(104. [21] LUO J, XIE C, ZHANG W, et al. Experimental mouse model of NMOSD produced by facilitated brain delivery of NMO-IgG by microbubble-enhanced low-frequency ultrasound in experimental allergic encephalomyelitis mice[J]. Mult Scler Relat Disord, 2020, 46(102473. [22] XIANG W, XIE C, LUO J, et al. Low Frequency Ultrasound With Injection of NMO-IgG and Complement Produces Lesions Different From Experimental Autoimmune Encephalomyelitis Mice[J]. Front Immunol, 2021, 12(727750. [23] ISHIKURA T, KINOSHITA M, SHIMIZU M, et al. Anti-AQP4 autoantibodies promote ATP release from astrocytes and induce mechanical pain in rats[J]. J Neuroinflammation, 2021, 18(1):181. [24] SAADOUN S, WATERS P, BELL B A, et al. Intra-cerebral injection of neuromyelitis optica immunoglobulin G and human complement produces neuromyelitis optica lesions in mice[J]. Brain, 2010, 133(Pt 2):349-61. [25] LEE C-L, WANG K-C, CHEN S-J, et al. Repetitive intrathecal injection of human NMO-IgG with complement exacerbates disease severity with NMO pathology in experimental allergic encephalomyelitis mice[J]. Mult Scler Relat Disord, 2019, 30(225-30. [26] ZHANG H, VERKMAN A S. Longitudinally extensive NMO spinal cord pathology produced by passive transfer of NMO-IgG in mice lacking complement inhibitor CD59[J]. J Autoimmun, 2014, 53(67-77. [27] ASAVAPANUMAS N, RATELADE J, VERKMAN A S. Unique neuromyelitis optica pathology produced in naïve rats by intracerebral administration of NMO-IgG[J]. Acta Neuropathol, 2014, 127(4):539-51. [28] MARIGNIER R, RUIZ A, CAVAGNA S, et al. Neuromyelitis optica study model based on chronic infusion of autoantibodies in rat cerebrospinal fluid[J]. J Neuroinflammation, 2016, 13(1):111. [29] HARADA K, FUJITA Y, OKUNO T, et al. Inhibition of RGMa alleviates symptoms in a rat model of neuromyelitis optica[J]. Sci Rep, 2018, 8(1):34. [30] GEIS C, RITTER C, RUSCHIL C, et al. The intrinsic pathogenic role of autoantibodies to aquaporin 4 mediating spinal cord disease in a rat passive-transfer model[J]. Exp Neurol, 2015, 265 [31] ZEKA B, HASTERMANN M, HOCHMEISTER S, et al. Highly encephalitogenic aquaporin 4-specific T cells and NMO-IgG jointly orchestrate lesion location and tissue damage in the CNS[J]. Acta Neuropathol, 2015, 130(6):783-98. [32] MATSUMOTO Y, KANAMORI A, NAKAMURA M, et al. Sera from patients with seropositive neuromyelitis optica spectral disorders caused the degeneration of rodent optic nerve[J]. Exp Eye Res, 2014, 119:61-9. -

计量
- 文章访问数: 26
- HTML全文浏览量: 5
- PDF下载量: 5
- 被引次数: 0