Institute of Health Sciences, Shanghai Jiao Tong University, School of Medicine, 200025 Shanghai, China.
Histochem Cell Biol. 2010 Mar;133(3):313-22. doi: 10.1007/s00418-009-0673-2.
To determine the possible involvement of neutrophils in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), we examined their infiltration pattern during the course of MOG35-55-induced EAE in the C57BL/6 mice. Using immunohistochemistry and flow cytometry, we found that the number of neutrophils was significantly increased during onset of disease, remained high at the peak stage and dramatically declined thereafter. Moreover, dual labeling provided anatomical evidence of a prominent accumulation of neutrophils in the center and vicinity of lesion areas of demyelination, axonal loss or axonal degeneration at early stages of EAE. These observations provide evidence that neutrophils are one of the major sources of inflammatory cells to initiate EAE, which suggest that neutrophils may contribute to demyelination and axonal degeneration in the acute phase of EAE and play a greater role than previously thought in the pathogenesis of EAE.
为了确定中性粒细胞在实验性自身免疫性脑脊髓炎（EAE）发病机制中的可能作用，我们在 C57BL/6 小鼠的 MOG35-55 诱导的 EAE 病程中检查了它们的浸润模式。通过免疫组织化学和流式细胞术，我们发现疾病发作时中性粒细胞数量明显增加，在高峰期保持高水平，此后急剧下降。此外，双重标记提供了解剖学证据，表明在 EAE 的早期阶段，大量中性粒细胞在脱髓鞘、轴突丢失或轴突变性的病变区域的中心和附近积聚。这些观察结果表明，中性粒细胞是引发 EAE 的主要炎症细胞来源之一，这表明中性粒细胞可能有助于 EAE 的急性期脱髓鞘和轴突变性，并在 EAE 的发病机制中发挥比以前认为的更大的作用。
