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Mediators of Inflammation
Volume 2017, Article ID 9340610, 6 pages
Research Article

Triggering Receptor Expressed on Myeloid Cells 2 Overexpression Inhibits Proinflammatory Cytokines in Lipopolysaccharide-Stimulated Microglia

1Department of Anesthesiology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, 182 Tongguan Road, Lianyungang 222000, China
2Department of Basic Medical Science, Kangda College, Nanjing Medical University, 88 Chunhui Road, Lianyungang 222000, China
3Department of Anesthesiology, Affiliated Drum Tower Hospital of Nanjing University Medical School, 321 Zhongshan Road, Nanjing 210008, China

Correspondence should be addressed to Jiying Feng; moc.361@dsyjgnef and Jinwei Zhang; moc.361@289wjz

Received 22 May 2017; Revised 21 August 2017; Accepted 28 September 2017; Published 18 October 2017

Academic Editor: Settimio Rossi

Copyright © 2017 Xiaobao Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Microglia play an important role in mediating inflammatory processes in the central nervous system (CNS). Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglia-specific receptor and could decrease neuropathology in Alzheimer’s disease (AD). However, the detailed mechanism remains unclear. This study was designed to elucidate the effect of TREM2 on microglia. We showed that lipopolysaccharide (LPS) stimulation significantly increases proinflammatory cytokines and suppressed TREM2 in microglia. In addition, TREM2 overexpression inhibited LPS-induced microglia activation and elevated M2 phenotype of microglia. Together, our results demonstrate that TREM2 overexpression reduced LPS-induced proinflammatory cytokine release in microglia and increased M2 phenotype of microglia. These findings provide novel insights that the regulation of microglia polarization may be an approach for ameliorating microglia inflammation in neurodegenerative diseases.