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Elevated Plasma Chemokines for Eosinophils in Neuromyelitis Optica Spectrum Disorders during Remission

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机构: [1]Department of Traditional Chinese Medicine, Beijing Tiantan Hospital, Capital Medical University, Beijing, China, [2]TCM Brain Research Institution, Beijing Tiantan Hospital, Capital Medical University, Beijing, China, [3]First Department of Neurology, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China, [4]School of Traditional Chinese Medicine, Capital Medical University, Beijing, China
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关键词: neuromyelitis optica spectrum disorders CCL13 relapse eotaxin eosinophil interleukin-1beta tumor necrosis factor-alpha

摘要:
Background: A prominent pathological feature of neuromyelitis optica spectrum disorders (NMOSD) is markedly greater eosinophilic infiltration than that seen in other demyelinating diseases, like multiple sclerosis (MS). Eosinophils express the chemokine receptor CCR3, which is activated by eotaxins (CCL11/eotaxin-1, CCL24/eotaxin-2, CCL26/eotaxin-3) and CCL13 [monocyte chemoattractant protein (MCP)-4]. Moreover, CCL13 is part of the chemokine set that activates CCR2. The present study aimed to evaluate plasma levels of eotaxins (CCL11, CCL24, and CCL26) and MCPs (CCL13, CCL2, CCL8, and CCL7) in patients with NMOSD during remission. Methods: Healthy controls (HC; n = 30) and patients with MS (n = 47) and NMOSD = 58) in remission were consecutively enrolled in this study between January 2016 and August 2017. Plasma CCLA 1, CCL24, CCL26, CCL2, CCL8, CCL7, CCL13, tumor necrosis factor (TNIF)-alpha, and interleukin (IL)-beta levels were detected using the human cytokine multiplex assay. Results: Plasma CCL13, CCL11, and CCL26 levels were all significantly higher in patients with NMOSD than in HC and patients with MS. No significant differences were found in the CCL13, CCL11, or CCL26 levels between patients with NMOSD receiving and not receiving immunosuppressive therapy. The plasma levels of TNF-alpha and IL-1 beta, which stimulate the above chemokines, were higher in patients with NMOSD than in HC. There was no difference in CCL24 levels among the three groups. In most cases, the CCL7 levels were below the threshold value of the human cytokine multiplex assay, which is in line with other studies. Adjusted multiple regression analyses showed a positive association of CCL13 levels with the number of relapses after controlling gender, age, body mass index, and disease duration in patients with NMOSD. Conclusion: The study indicates that in NMOSD, the overproduction of cytokines such as IL-beta and TNF-alpha during remission stimulates eosinophilic chemoattractants such as CCL13, CCL11, and CCL26, which in turn bind to their receptor (CCR3); this could lead to eosinophil hypersensitivity. These findings suggest that the elevated secretion of CCL13, CCL11, and CCL26 may be a critical step in eosinophil recruitment during NMOSD remission.

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出版当年[2017]版:
大类 | 2 区 医学
小类 | 3 区 临床神经病学 3 区 神经科学
最新[2023]版:
大类 | 3 区 医学
小类 | 3 区 临床神经病学 3 区 神经科学
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出版当年[2016]版:
Q2 CLINICAL NEUROLOGY Q2 NEUROSCIENCES
最新[2023]版:
Q2 CLINICAL NEUROLOGY Q3 NEUROSCIENCES

影响因子: 最新[2023版] 最新五年平均 出版当年[2016版] 出版当年五年平均 出版前一年[2015版] 出版后一年[2017版]

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第一作者机构: [1]Department of Traditional Chinese Medicine, Beijing Tiantan Hospital, Capital Medical University, Beijing, China, [2]TCM Brain Research Institution, Beijing Tiantan Hospital, Capital Medical University, Beijing, China,
通讯作者:
通讯机构: [1]Department of Traditional Chinese Medicine, Beijing Tiantan Hospital, Capital Medical University, Beijing, China, [2]TCM Brain Research Institution, Beijing Tiantan Hospital, Capital Medical University, Beijing, China,
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