Interleukin-33 Protects Ischemic Brain Injury by Regulating Specific Microglial Activities.

Abstract

Interleukin-33 (IL-33), a novel member of the IL-1 family, expressed in many tissue and cell types, is involved in inflammation and immune functions. Previous studies suggest that IL-33 may play a role in ischemic stroke. Here, we evaluated the effect of IL-33 in cerebral ischemia-reperfusion-induced injury and investigated its underlying mechanism. Our data indicated that IL-33 deficiency exacerbated the neurological dysfunction caused by cerebral ischemia-reperfusion injury in mice and led to the formation of larger cerebral infarct volume as shown by 2,3,5-triphenyltetrazolium chloride staining and magnetic resonance imaging. Furthermore, the M1 and M2 macrophage-like microglial immune responses with decreased expression of the corresponding cytokines were seen in IL-33-deficient mice. IL-33 deficiency led to more biased to M2-like activities. The aggravated cerebral ischemia-reperfusion injury in IL-33-deficient mice is partially restored by intracerebroventricular injection of IL-33. These data suggest that IL-33 promotes the amplification of macrophage polarization and cytokine production associated with M2 macrophage-like microglial immune phenotype, which may contribute to the protective effects in the ischemic stroke, and that IL-33 may be a potential therapeutic target for ischemic stroke.

• Authors: Qianping Luo, Yong Fan, Lili Lin, Jingjing Wei, Zuanfang Li, Yongkun Li, Susumu Nakae, Wei Lin, Qi Chen
• Journal: Neuroscience (Neuroscience) Vol. 385 Pg. 75-89 (08 10 2018) ISSN: 1873-7544 [Electronic] United States
• PMID: 29906552 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2018 IBRO. Published by Elsevier Ltd. All rights reserved.

Chemical References

• Cytokines
• Interleukin-33

Topics

• Animals
• Brain (drug effects, metabolism)
• Brain Ischemia (drug therapy, genetics, metabolism)
• Cytokines (metabolism)
• Interleukin-33 (genetics, metabolism, pharmacology, therapeutic use)
• Macrophages (drug effects, metabolism)
• Male
• Mice
• Mice, Knockout
• Microglia (drug effects, metabolism)
• Reperfusion Injury (drug therapy, genetics, metabolism)