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Tytuł pozycji:

RAGE and CCR7 mediate the transmigration of Zika-infected monocytes through the blood-brain barrier.

Tytuł:
RAGE and CCR7 mediate the transmigration of Zika-infected monocytes through the blood-brain barrier.
Autorzy:
de Carvalho GC; Département de Biologie, Faculté des Sciences, Université de Sherbrooke, 2500 boul de l'Université, Sherbrooke, QC, Canada; Laboratory of Dermatology and Immunodeficiencies, LIM-56, Department of Dermatology, Medical School, Institute of Tropical Medicine, University of São Paulo, São Paulo, Brazil.
Borget MY; Département de Biologie, Faculté des Sciences, Université de Sherbrooke, 2500 boul de l'Université, Sherbrooke, QC, Canada.
Bernier S; Département de Biologie, Faculté des Sciences, Université de Sherbrooke, 2500 boul de l'Université, Sherbrooke, QC, Canada.
Garneau D; Département de Biologie, Faculté des Sciences, Université de Sherbrooke, 2500 boul de l'Université, Sherbrooke, QC, Canada.
da Silva Duarte AJ; Laboratory of Dermatology and Immunodeficiencies, LIM-56, Department of Dermatology, Medical School, Institute of Tropical Medicine, University of São Paulo, São Paulo, Brazil.
Dumais N; Département de Biologie, Faculté des Sciences, Université de Sherbrooke, 2500 boul de l'Université, Sherbrooke, QC, Canada. Electronic address: .
Źródło:
Immunobiology [Immunobiology] 2019 Nov; Vol. 224 (6), pp. 792-803. Date of Electronic Publication: 2019 Aug 25.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Publication: <2005->: Amsterdam : Elsevier
Original Publication: Stuttgart ; New York, Fischer.
MeSH Terms:
Zika Virus Infection*
Antigens, Neoplasm/*physiology
Blood-Brain Barrier/*physiology
Chemokine CCL19/*physiology
HMGB1 Protein/*physiology
Mitogen-Activated Protein Kinases/*physiology
Monocytes/*physiology
Receptors, CCR7/*physiology
Animals ; Cell Line ; Cell Movement ; Chlorocebus aethiops ; Endothelial Cells/physiology ; Humans ; Monocytes/virology ; Zika Virus
Contributed Indexing:
Keywords: Blood-brain barrier; CCR7; HMGB1; Monocytes; RAGE; Zika virus
Substance Nomenclature:
0 (Antigens, Neoplasm)
0 (CCL19 protein, human)
0 (CCR7 protein, human)
0 (Chemokine CCL19)
0 (HMGB1 Protein)
0 (HMGB1 protein, human)
0 (Receptors, CCR7)
EC 2.7.11.22 (MOK protein, human)
EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
Entry Date(s):
Date Created: 20190909 Date Completed: 20200424 Latest Revision: 20200424
Update Code:
20240105
DOI:
10.1016/j.imbio.2019.08.007
PMID:
31493920
Czasopismo naukowe
Details of the "Trojan Horse" mechanism by which Zika virus (ZIKV) crosses the blood-brain barrier (BBB) remain unclear. However, the migration of ZIKV-infected monocytes to the brain is thought to be dependent on both pattern-recognition and chemokine receptors. In this study, we investigated whether the migration of ZIKV-infected MonoMac-1 (MM-1) cells through the BBB is dependent on chemokine receptor 7 (CCR7) and receptor for advanced glycation end (RAGE); we also determined whether high mobility group box protein 1 (HMGB1) could facilitate the permeabilization of endothelial cells. We demonstrated that ZIKV infects MM-1 cells, leading to milieu accumulation of HMGB1. Our results suggest that HMGB1 is involved in the dysregulation of primary human brain microvascular endothelial cell junction markers. Our results also indicate that the migration of ZIKV-infected monocytes is dependent on chemokine ligand 19 (CCL19), the natural ligand of CCR7, in conditions recapitulating inflammation. RAGE-dependent migration of ZIKV-infected cells declined during transmigration assays in the presence of RAGE receptor antagonist FPS-ZM1. Understanding the molecular role of monocyte trafficking during ZIKV infections could facilitate the development of new therapeutic strategies to prevent the deleterious consequences of ZIKV neuroinfection.
(Copyright © 2019 Elsevier GmbH. All rights reserved.)

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