Promotion of microglial phagocytosis by tuftsin stimulates remyelination in experimental autoimmune encephalomyelitis Corrigendum in /10.3892/mmr.2020.11042

Bao,Zheng; Hao,Jinqi; Li,Yuhong; Feng,Fumin

doi:10.3892/mmr.2019.10788

Promotion of microglial phagocytosis by tuftsin stimulates remyelination in experimental autoimmune encephalomyelitis

Corrigendum in: /10.3892/mmr.2020.11042

Authors:
- Zheng Bao
- Jinqi Hao
- Yuhong Li
- Fumin Feng
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Affiliations: School of Public Health, North China University of Science and Technology, Tangshan, Hebei 063210, P.R. China, School of Public Health, BaoTou Medical College, Baotou, Neimenggu 014040, P.R. China
Published online on: October 31, 2019 https://doi.org/10.3892/mmr.2019.10788
Pages: 5190-5196
Copyright: © Bao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Microglia were once thought to serve a pathogenic role in demyelinating diseases, particularly in multiple sclerosis (MS). However, it has recently been shown that in the experimental autoimmune encephalomyelitis (EAE) model of MS, microglia could serve a protective role by promoting remyelination via the efficient removal of apoptotic cells, the phagocytosis of debris and the support of myelinating oligodendrocytes. The aim of the present study was to determine if the effect of microglia could promote the recovery of EAE and attenuate symptoms in EAE. The severity of EAE was assessed by clinical scores, pathologic changes revealed by luxol fast blue staining and immunohistochemical techniques. The results suggested that microglia reduced clinical scores in mice, suppressed ongoing severe EAE and promoted remyelination and recovery in EAE mice. In addition, following induction with tuftsin, the M1/M2 cytokine balance was shifted, downregulating the proinflammatory M1 response and upregulating the anti‑inflammatory M2 response. Generally, microglia can stimulate remyelination, which serves a protective role in different phases of EAE and may represent a potential therapeutic strategy for the treatment of MS.

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