Peripheral challenge with a viral mimic upregulates expression of the complement genes in the hippocampus

被引：17

作者：

Michalovicz, Lindsay T. ^{[1
]}

Lally, Brent ^{[1
]}

Konat, Gregory W. ^{[1
]}

机构：

[1] W Virginia Univ, Sch Med, Dept Neurobiol & Anat, Morgantown, WV 26506 USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2015年 / 285卷

基金：

美国国家卫生研究院;

关键词：

Polyinosinic-polycytidylic acid; Inflammation; Hippocampus; Complement system; Transcriptome; Immunofluorescence; MOTOR CORTEX EXCITABILITY; INFLAMMATORY RESPONSE; CIRCULATING ENDOTOXIN; ALZHEIMERS-DISEASE; PATHWAY; BRAIN; INFECTIONS; ACTIVATION; CYTOKINE; CNS;

D O I：

10.1016/j.jneuroim.2015.06.003

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Peripheral challenge with a viral mimetic, polyinosinic-polycytidylic acid (PIC) induces hippocampal hyperexcitability in mice. Here, we characterized this hippocampal response through a whole genome transcriptome analysis. Intraperitoneal injection of PIC resulted in temporal dysregulation of 625 genes in the hippocampus, indicating an extensive genetic reprogramming. The bioinformatics analysis of these genes revealed the complement pathway to be the most significantly activated. The gene encoding complement factor B (CfB) exhibited the highest response, and its upregulation was commensurate with the development of hyperexcitability. Collectively, these results suggest that the induction of hippocampal hyperexcitability may be mediated by the alternative complement cascades. (C) 2015 Elsevier B.V. All rights reserved.

引用

页码：137 / 142

页数：6

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