Blockade of IL-17A/IL-17R Pathway Protected Mice from Sepsis-Associated Encephalopathy by Inhibition of Microglia Activation.
Animals
Antibodies
/ therapeutic use
Brain
/ drug effects
Cells, Cultured
Cognitive Dysfunction
/ physiopathology
Disease Models, Animal
Fluorescent Antibody Technique
Interleukin-17
/ antagonists & inhibitors
Male
Mice
Mice, Inbred C57BL
Microglia
/ drug effects
Receptors, Interleukin-17
/ antagonists & inhibitors
Sepsis-Associated Encephalopathy
/ metabolism
Signal Transduction
/ drug effects
Journal
Mediators of inflammation
ISSN: 1466-1861
Titre abrégé: Mediators Inflamm
Pays: United States
ID NLM: 9209001
Informations de publication
Date de publication:
2019
2019
Historique:
received:
04
01
2019
revised:
06
05
2019
accepted:
27
05
2019
entrez:
6
11
2019
pubmed:
7
11
2019
medline:
9
4
2020
Statut:
epublish
Résumé
Sepsis-associated encephalopathy (SAE) is a poorly understood condition that leads to long-term cognitive impairment and increased mortality in survivors. Recent research revealed that IL-17A/IL-17R might serve as a checkpoint in microglia-mediated neuroinflammation. The present study was designed to determine the specific role of IL-17A-mediated microglia activation in the development of SAE. A mouse model of SAE was induced by cecal ligation and puncture (CLP), and behavior performance was evaluated by the inhibitory avoidance test and the open field test. Cytokine expression and microglia activation in brain tissue were determined at 6 h, 12 h, 24 h, 48 h, and day 7 post surgery. Further, septic mice were intracerebral ventricle- (i.c.v.-) injected with recombinant IL-17A, anti-IL-17A ab, anti-IL-17R ab, or isotype controls to evaluate the potential effects of IL-17A/IL-17R blockade in the prevention of SAE. Septic peritonitis induced significant impairment of learning memory and exploratory activity, which was associated with a higher expression of IL-17A, IL-1
Identifiants
pubmed: 31686986
doi: 10.1155/2019/8461725
pmc: PMC6800921
doi:
Substances chimiques
Antibodies
0
IL17A protein, human
0
Il17ra protein, mouse
0
Interleukin-17
0
Receptors, Interleukin-17
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
8461725Informations de copyright
Copyright © 2019 Bo Ye et al.
Déclaration de conflit d'intérêts
The authors have not disclosed any potential conflicts of interest.
Références
Ann Neurol. 1993 Jan;33(1):94-100
pubmed: 8388191
JAMA. 2010 Oct 27;304(16):1787-94
pubmed: 20978258
J Neuropathol Exp Neurol. 1999 Oct;58(10):1078-89
pubmed: 10515231
Lancet Respir Med. 2015 Jan;3(1):61-9
pubmed: 25434614
J Neuroimmunol. 2008 Feb;194(1-2):54-61
pubmed: 18164424
Neurol India. 2018 Mar-Apr;66(2):352-361
pubmed: 29547154
Biomed Res Int. 2014;2014:245210
pubmed: 25054133
Auton Neurosci. 2000 Dec 20;85(1-3):60-5
pubmed: 11189027
Trends Neurosci. 2002 Mar;25(3):154-9
pubmed: 11852148
Gene. 2017 May 30;614:8-14
pubmed: 28122268
Bio Protoc. 2016 Nov 5;6(21):null
pubmed: 29104890
Acta Neuropathol. 2015 May;129(5):625-37
pubmed: 25716179
Brain Behav Immun. 2015 Jan;43:54-9
pubmed: 25019583
Clin Microbiol Infect. 2013 Jun;19(6):510-2
pubmed: 23397980
Annu Rev Immunol. 2014;32:367-402
pubmed: 24471431
J Immunol. 2004 Sep 15;173(6):3916-24
pubmed: 15356140
Neurobiol Aging. 2014 Jan;35(1):109-21
pubmed: 23993702
Lancet. 2018 Jul 7;392(10141):75-87
pubmed: 29937192
PLoS One. 2012;7(10):e46506
pubmed: 23056325
Acad Emerg Med. 2008 May;15(5):399-413
pubmed: 18439194
Neuroscience. 2011 Mar 10;176:162-72
pubmed: 21182899
Annu Rev Immunol. 2009;27:485-517
pubmed: 19132915
Glia. 2010 May;58(7):839-47
pubmed: 20091781
Curr Neurovasc Res. 2014;11(3):262-70
pubmed: 24845857
Can J Neurol Sci. 2003 May;30(2):98-105
pubmed: 12774948
Front Immunol. 2017 Jun 16;8:597
pubmed: 28670310
Adv Exp Med Biol. 1999;461:25-46
pubmed: 10442165
Brain Behav Immun. 2010 May;24(4):641-51
pubmed: 20138983
Crit Care Med. 2005 Jan;33(1):221-3; discussion 262-3
pubmed: 15644673
Nat Rev Neurol. 2012 Oct;8(10):557-66
pubmed: 22986430