Abstract
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.
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Acknowledgments
This work was supported by grants from National Natural Science Foundation of China (30671926) and Shanghai Commission of Science and Technology (06ZR14164). The authors would like to thank Taylor Guo for critical reading of the manuscript. We are grateful to Qi Zhang for help with excellent technical support on the EAE induction.
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F. Wu and W. Cao contributed equally to this work.
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Wu, F., Cao, W., Yang, Y. et al. Extensive infiltration of neutrophils in the acute phase of experimental autoimmune encephalomyelitis in C57BL/6 mice. Histochem Cell Biol 133, 313–322 (2010). https://doi.org/10.1007/s00418-009-0673-2
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DOI: https://doi.org/10.1007/s00418-009-0673-2