Increased Levels of IL-16 in the Central Nervous System during Neuroinflammation Are Associated with Infiltrating Immune Cells and Resident Glial Cells.
Increased Levels of IL-16 in the Central Nervous System during Neuroinflammation Are Associated with Infiltrating Immune Cells and Resident Glial Cells.
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DOI：
10.3390/biology10060472
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发表时间：
2021-05-27
期刊：
影响因子：
4.2
通讯作者：
Jiang HR
中科院分区：
文献类型：
--
作者：
Hridi SU;Barbour M;Wilson C;Franssen AJ;Harte T;Bushell TJ;Jiang HR
白细胞介素-16是一种参与某些免疫细胞迁移的蛋白质，在多发性硬化症（一种影响中枢神经系统的炎性脱髓鞘疾病，脑和脊髓）。目前，尚不完全清楚哪些细胞在中枢神经系统的炎症反应期间产生白细胞介素-16。本研究使用多发性硬化症小鼠模型，调查白细胞介素-16的表达水平与神经炎症严重程度之间的相关性，并确定产生白细胞介素-16的细胞。我们的数据显示，与对照组相比，小鼠模型的脑和脊髓组织中白细胞介素-16的表达水平显著增加。此外，其他免疫测定揭示，在中枢神经系统病变中表达白细胞介素-16的细胞数量显著增加，可能是浸润性免疫细胞和常驻神经胶质细胞，而不是神经元。我们的研究结果表明，白细胞介素-16是密切参与的病理多发性硬化症和其他炎症性疾病的中枢神经系统通过胶质细胞和浸润的免疫细胞。白细胞介素（IL）-16是一种CD 4+免疫细胞特异性趋化细胞因子，已被证明参与多发性硬化症的发展，多发性硬化症是中枢神经系统（CNS）的炎性脱髓鞘疾病。虽然据报道免疫细胞如T细胞和巨噬细胞是IL-16的生产者，但CNS中IL-16的细胞来源尚不清楚。本研究探讨了中枢神经系统中IL-16表达水平与神经炎症严重程度的相关性，并确定了实验性自身免疫性脑脊髓炎（EAE）小鼠中枢神经系统中产生IL-16的细胞表型。我们的数据显示，与磷酸盐缓冲盐水（PBS）免疫对照相比，IL-16表达在EAE小鼠的脑和脊髓组织中显著增加。双重免疫荧光染色显示，EAE小鼠CNS病变中显著增加的IL-16+细胞可能是CD 45+浸润的免疫细胞如CD 4+或F4/80+细胞以及CNS驻留的CD 11b+小胶质细胞和GFAP+星形胶质细胞，而不是NeuN+神经元。我们的数据表明细胞因子IL-16与EAE病理密切相关，如其在神经胶质细胞和浸润免疫细胞中表达增加所证明的，这影响了神经炎症中CD 4+免疫细胞的募集和活化。
Interleukin-16 is a protein involved in the migration of some immune cells and plays an important role in the development of multiple sclerosis, an inflammatory demyelinating disease that affects the central nervous system (i.e., brain and spinal cord). Currently, it is not fully understood which cells produce interleukin-16 during the inflammatory response in the central nervous system. This study investigates the correlation between the expression levels of interleukin-16 and the severity of neuroinflammation and determines the cells which produce interleukin-16, using a mouse model of multiple sclerosis. Our data show that the expression levels of interleukin-16 are significantly increased in the brain and spinal cord tissues of the mouse model compared to controls. Furthermore, other immune assays reveal that the significantly increased number of cells expressing interleukin-16 in the central nervous system lesions are likely to be infiltrating immune cells and resident glial cells, but not neurons. Our findings suggest that interleukin-16 is closely involved in the pathology of multiple sclerosis and other inflammatory diseases in the central nervous system via the glial and infiltrating immune cells. Interleukin (IL)-16, a CD4+ immune cell specific chemoattractant cytokine, has been shown to be involved in the development of multiple sclerosis, an inflammatory demyelinating disease of the central nervous system (CNS). While immune cells such as T cells and macrophages are reported to be the producers of IL-16, the cellular source of IL-16 in the CNS is less clear. This study investigates the correlation of IL-16 expression levels in the CNS with the severity of neuroinflammation and determines the phenotype of cells which produce IL-16 in the CNS of experimental autoimmune encephalomyelitis (EAE) mice. Our data show that IL-16 expression is significantly increased in the brain and spinal cord tissues of EAE mice compared to phosphate buffered saline (PBS) immunised controls. Dual immunofluorescence staining reveals that the significantly increased IL-16+ cells in the CNS lesions of EAE mice are likely to be the CD45+ infiltrating immune cells such as CD4+ or F4/80+ cells and the CNS resident CD11b+ microglia and GFAP+ astrocytes, but not NeuN+ neurons. Our data suggest cytokine IL-16 is closely involved in EAE pathology as evidenced by its increased expression in the glial and infiltrating immune cells, which impacts the recruitment and activation of CD4+ immune cells in the neuroinflammation.
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