视神经脊髓炎
渗透(HVAC)
病态的
趋化因子
免疫学
病理
小胶质细胞
炎症
光谱紊乱
髓鞘
脱髓鞘病
脱髓鞘病
医学
中枢神经系统
多发性硬化
内科学
物理
精神科
热力学
作者
Zhuhe Liu,Yuanyuan Wang,Yuewen Ding,Haitao Wang,Jun Zhang,Honghao Wang
标识
DOI:10.1016/j.clim.2022.109139
摘要
Neuromyelitis optica spectrum disorder (NMOSD) is an inflammatory demyelinating disease of the central nervous system (CNS). Our previous study indicated that neutrophil-related chemokine CXCL7 is elevated in the cerebrospinal fluid (CSF) of NMOSD patients. To study the potential function of CXCL7 during NMOSD, we measured the chemokines level in CSF of follow-up patients, and established three NMOSD mouse models by injecting aquaporin4 (AQP4)-IgG. Astrocytes loss, inflammatory infiltration, and myelin sheath damage were detected by western blot or immunofluorescence analysis. We found CXCL7 was significantly increased in the serum and CSF of model mice, and exogenous CXCL7 caused serious astrocyte injury, obvious microglia activation, and increased infiltration of neutrophils and macrophages, resulting in secondary demyelination. Consistently, knocking down the CXCL7 reversed the loss of AQP4, and attenuated the inflammatory response. Collectively, our data indicates that CXCL7 aggravates NMOSD-like pathological damage to astrocytes and myelin sheath mainly via promoting neuroinflammatory response.
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