Transitory loss of glia and the subsequent modulation in inflammatory cytokines/chemokines regulate paracellular claudin-5 expression in endothelial cells

被引：23
作者：
Camire, Ryan B. [1 ]
Beaulac, Holly J. [2 ,3 ]
Willis, Colin L. [2 ,3 ]
机构：
[1] Univ New England, Westbrook Coll Hlth Profess, Biddeford, ME 04005 USA
[2] Univ New England, Coll Osteopath Med, Dept Biomed Sci, Biddeford, ME 04005 USA
[3] Univ New England, Ctr Excellence Neurosci, Biddeford, ME 04005 USA
来源：
JOURNAL OF NEUROIMMUNOLOGY | 2015年 / 284卷
基金：
美国国家卫生研究院;
关键词：
Astrocytes; Blood brain barrier; Chemokine; Cytokine; Claudin-5; Microglia; BLOOD-BRAIN-BARRIER; NECROSIS-FACTOR-ALPHA; JUNCTION PROTEIN EXPRESSION; TIGHT JUNCTION; TNF-ALPHA; INTERLEUKIN-6; PERMEABILITY; ASTROCYTES; MICROGLIA; PAIN;
D O I：
10.1016/j.jneuroim.2015.05.008
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Signaling mechanisms involved in regulating blood-brain barrier (BBB) integrity during central nervous system (CNS) inflammation remain unclear. We show that an imbalance between pro-/anti-inflammatory cytokines/chemokines alters claudin-5 expression. In vivo, gliotoxin-induced changes in glial populations and an imbalance between pro-/anti-inflammatory cytokine/chemokine expression occurred as BBB integrity was compromised. The balance was restored as BBB integrity was re-established. In vitro, TNF-alpha, IL-6, and MCP-1 induced paracellular claudin-5 expression loss. TNF-alpha- and IL-6- effects were mediated through the P13K pathway and IL-10 attenuated TNF-alpha's effect. This study shows that pro-/anti-inflammatory modulators play a critical role in BBB integrity during CNS inflammation. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码：57 / 66
页数：10
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