Chitinase effects on immune cell response in neuromyelitis optica and multiple sclerosis
Chitinase effects on immune cell response in neuromyelitis optica and multiple sclerosis
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DOI：
10.1177/1352458510392619
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发表时间：
2011-05-01
影响因子：
5.8
通讯作者：
Fiol, Marcela
中科院分区：
文献类型：
--
作者：
Correale, Jorge;Fiol, Marcela
背景资料：目的：探讨几丁质酶在多发性硬化（MS）和视神经肌萎缩症（NMO）中的作用。方法：采用免疫组化方法检测多发性硬化（MS）和视神经肌萎缩症（NMO）患者的几丁质酶活性。使用ELISA测量壳三糖苷酶、酸性哺乳动物几丁质酶（AMCase）和几丁质酶3-样-1（CHI 3L 1）的水平，在来自24名复发缓解型（RR）MS患者、24名继发进行型（SP）MS患者、12名NMO患者、24名其他炎性神经系统疾病（OIND）患者和24名健康对照（HC）的脑脊液（CSF）和血清中，使用ELISPOT研究抗MOG精氨酸分泌细胞的数量。使用ELISA评估嗜酸性粒细胞趋化因子、MCP-1、RANTES和IL-8。使用体外血脑屏障（BBB）模型，在存在和不存在的chitinases.Results：CSF几丁质酶水平显着增加与RRMS和NMO患者相比，HC和SPMS和OIND患者的细胞transmigration测定。与此相反，没有显着差异，血清几丁质酶水平检测组之间。CSF几丁质酶水平显示与抗MOG IL-13产生细胞和嗜酸性粒细胞趋化因子水平相关。体外实验显示，IL-13显著增加巨噬细胞几丁质酶分泌，但IL-5、IL-6、IL-12或IFN-γ不显著增加巨噬细胞几丁质酶分泌。此外，几丁质酶增强IL-8，RANTES，MCP-1，和嗜酸性粒细胞活化趋化因子的生产，增加迁移能力的嗜酸性粒细胞，T细胞，巨噬细胞在体外BBB model.Conclusions：几丁质酶增加在脑脊液中的NMO患者在响应IL-13。这些增强的水平可能通过增加免疫细胞穿过BBB的迁移而导致中枢神经系统炎症。
Background: Recent studies conducted in arthritis, asthma, and inflammatory bowel disease suggest that chitinases are important in inflammatory processes and tissue remodeling.Objective: To investigate the role of chitinases in multiple sclerosis (MS) and neuromyelitis optica (NMO).Methods: Levels of chitotriosidase, acid mammalian chitinase (AMCase), and chitinase 3-like-1 (CHI3L1) were measured using ELISA, in cerebrospinal fluid (CSF) and in serum from 24 patients with relapsing remitting (RR) MS, 24 patients with secondary progressive (SP) MS, 12 patients with NMO, 24 patients with other inflammatory neurological diseases (OIND), and 24 healthy controls (HCs). The number of anti-MOG cytokine-secreting cells was studied using ELISPOT. Eotaxins, MCP-1, RANTES, and IL-8 were assessed using ELISA. Cell transmigration was determined using an in vitro blood-brain barrier (BBB) model, in the presence and absence of chitinases.Results: CSF chitinase levels were significantly increased in patients with RRMS and NMO compared with HCs and patients with SPMS and OIND. In contrast, no significant differences were detected in serum chitinase levels between groups. Chitinase CSF levels showed correlation with anti-MOG IL-13-producing cells, and eotaxin levels. In vitro experiments showed macrophage chitinase secretion was significantly increased by IL-13, but not by IL-5, IL-6, IL-12, or IFN-gamma. Moreover, chitinases enhanced IL-8, RANTES, MCP-1, and eotaxin production, increasing migratory capacity in eosinophils, T cells, and macrophages across an in vitro BBB model.Conclusions: Chitinases increased in the CSF from patients with NMO in response to IL-13. These enhanced levels could contribute to central nervous system inflammation by increasing immune cell migration across the BBB.