IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury.

Mice Humans Animals Interleukin-17 / metabolism White Matter / metabolism Endothelial Cells / metabolism Brain / metabolism Signal Transduction Brain Injuries / metabolism Oligodendroglia / metabolism Chemokine CXCL5 / metabolism
CP: Immunology CP: Neuroscience CXCL5 IL-17 cerebral small vessel disease high-fat diet inflammation obesity stroke white matter

Journal

Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691

Informations de publication

Date de publication:
20 12 2022
Historique:
received: 31 10 2021
revised: 10 10 2022
accepted: 28 11 2022
entrez: 21 12 2022
pubmed: 22 12 2022
medline: 24 12 2022
Statut: ppublish

Résumé

Cerebral small vessel disease and brain white matter injury are worsened by cardiovascular risk factors including obesity. Molecular pathways in cerebral endothelial cells activated by chronic cerebrovascular risk factors alter cell-cell signaling, blocking endogenous and post-ischemic white matter repair. Using cell-specific translating ribosome affinity purification (RiboTag) in white matter endothelia and oligodendrocyte progenitor cells (OPCs), we identify a coordinated interleukin-chemokine signaling cascade within the oligovascular niche of subcortical white matter that is triggered by diet-induced obesity (DIO). DIO induces interleukin-17B (IL-17B) signaling that acts on the cerebral endothelia through IL-17Rb to increase both circulating and local endothelial expression of CXCL5. In white matter endothelia, CXCL5 promotes the association of OPCs with the vasculature and triggers OPC gene expression programs regulating cell migration through chemokine signaling. Targeted blockade of IL-17B reduced vessel-associated OPCs by reducing endothelial CXCL5 expression. In multiple human cohorts, blood levels of CXCL5 function as a diagnostic and prognostic biomarker of vascular cognitive impairment.

Identifiants

DOI: 10.1016/j.celrep.2022.111848 PMID: 36543124 PMC: PMC10026849
pubmed: 36543124
pii: S2211-1247(22)01740-5
doi: 10.1016/j.celrep.2022.111848
pmc: PMC10026849
mid: NIHMS1860004
pii:
doi:

Substances chimiques

Interleukin-17 0
CXCL5 protein, human 0
Chemokine CXCL5 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

111848

Subventions

Organisme : NINDS NIH HHS
ID : K08 NS083740
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG010129
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK041301
Pays : United States
Organisme : NINDS NIH HHS
ID : RF1 NS114336
Pays : United States

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The Regents of the University of California have filed a patent entitled “Serologic Detection of Silent Brain Ischemia” based on this work. G.X. and J.D.H. are co-inventors on this patent. J.D.H. is the founder of Sage Cerebrovascular Diagnostics, Inc.

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Auteurs

Guanxi Xiao (G)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.

Rosie Kumar (R)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.

Yutaro Komuro (Y)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.

Jasmine Burguet (J)

Institut Jean-Pierre Bourgin, INRA, AgroParisTech, CNRS, Université Paris-Saclay, 78000 Versailles, France.

Visesha Kakarla (V)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.

Ida Azizkhanian (I)

New York Medical College, School of Medicine, Valhalla, NY, USA.

Sunil A Sheth (SA)

Department of Neurology, UT Health McGovern School of Medicine, Houston, TX, USA.

Christopher K Williams (CK)

Department of Neuropathology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.

Xinhai R Zhang (XR)

Department of Neuropathology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.

Michal Macknicki (M)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.

Andrew Brumm (A)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.

Riki Kawaguchi (R)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA; Department of Psychiatry, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, CA, USA.

Phu Mai (P)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.

Naoki Kaneko (N)

Department of Radiological Sciences, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.

Harry V Vinters (HV)

Department of Neuropathology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.

S Thomas Carmichael (ST)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.

Leif A Havton (LA)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA; Department of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.

Charles DeCarli (C)

Department of Neurology, University of California, Davis, Davis, CA, USA.

Jason D Hinman (JD)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA. Electronic address: jhinman@mednet.ucla.edu.

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Classifications MeSH

questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › IL-17/CXCL5 signaling within the oligovascular...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Primates › Haplorhini › Catarrhini › Hominidae › Humains › IL-17/CXCL5 signaling within the oligovascular...
questionsmedicales.fr › Eucaryotes › Animaux › IL-17/CXCL5 signaling within the oligovascular...
questionsmedicales.fr › Facteurs biologiques › Protéines et peptides de signalisation intercellulaire › Cytokines › Interleukines › Interleukine-17 › IL-17/CXCL5 signaling within the oligovascular...
questionsmedicales.fr › Système nerveux › Système nerveux central › Moelle spinale › Substance blanche › IL-17/CXCL5 signaling within the oligovascular...
questionsmedicales.fr › Cellules › Cellules épithéliales › Cellules endothéliales › IL-17/CXCL5 signaling within the oligovascular...
questionsmedicales.fr › Système nerveux › Système nerveux central › Encéphale › IL-17/CXCL5 signaling within the oligovascular...
questionsmedicales.fr › Phénomènes physiologiques cellulaires › Transduction du signal › IL-17/CXCL5 signaling within the oligovascular...
questionsmedicales.fr › Plaies et blessures › Traumatismes du système nerveux › Traumatismes cranioencéphaliques › Lésions encéphaliques › IL-17/CXCL5 signaling within the oligovascular...
questionsmedicales.fr › Cellules › Névroglie › Oligodendroglie › IL-17/CXCL5 signaling within the oligovascular...
questionsmedicales.fr › Facteurs biologiques › Protéines et peptides de signalisation intercellulaire › Cytokines › Chimiokines › Chimiokines CXC › Chimiokine CXCL5 › IL-17/CXCL5 signaling within the oligovascular...