DHEA Inhibits Leukocyte Recruitment through Regulation of the Integrin Antagonist DEL-1.
Animals
CCAAT-Enhancer-Binding Protein-beta
/ immunology
CD18 Antigens
/ immunology
Calcium-Binding Proteins
/ immunology
Cell Adhesion
/ immunology
Cell Adhesion Molecules
/ immunology
Dehydroepiandrosterone
/ pharmacology
Endothelium, Vascular
/ immunology
Female
Gene Expression Regulation
/ immunology
Leukocytes
/ cytology
Mice
Phosphatidylinositol 3-Kinases
/ immunology
Promoter Regions, Genetic
/ immunology
Proto-Oncogene Proteins c-akt
/ immunology
Receptor, trkA
/ immunology
Signal Transduction
/ immunology
Journal
Journal of immunology (Baltimore, Md. : 1950)
ISSN: 1550-6606
Titre abrégé: J Immunol
Pays: United States
ID NLM: 2985117R
Informations de publication
Date de publication:
01 03 2020
01 03 2020
Historique:
received:
02
07
2019
accepted:
27
12
2019
pubmed:
26
1
2020
medline:
9
9
2020
entrez:
26
1
2020
Statut:
ppublish
Résumé
Leukocytes are rapidly recruited to sites of inflammation via interactions with the vascular endothelium. The steroid hormone dehydroepiandrosterone (DHEA) exerts anti-inflammatory properties; however, the underlying mechanisms are poorly understood. In this study, we show that an anti-inflammatory mechanism of DHEA involves the regulation of developmental endothelial locus 1 (DEL-1) expression. DEL-1 is a secreted homeostatic factor that inhibits β2-integrin-dependent leukocyte adhesion, and the subsequent leukocyte recruitment and its expression is downregulated upon inflammation. Similarly, DHEA inhibited leukocyte adhesion to the endothelium in venules of the inflamed mouse cremaster muscle. Importantly, in a model of lung inflammation, DHEA limited neutrophil recruitment in a DEL-1-dependent manner. Mechanistically, DHEA counteracted the inhibitory effect of inflammation on DEL-1 expression. Indeed, whereas TNF reduced DEL-1 expression and secretion in endothelial cells by diminishing C/EBPβ binding to the
Identifiants
pubmed: 31980574
pii: jimmunol.1900746
doi: 10.4049/jimmunol.1900746
pmc: PMC7026770
doi:
Substances chimiques
CCAAT-Enhancer-Binding Protein-beta
0
CD18 Antigens
0
Calcium-Binding Proteins
0
Cebpb protein, mouse
0
Cell Adhesion Molecules
0
Edil3 protein, mouse
0
Dehydroepiandrosterone
459AG36T1B
Receptor, trkA
EC 2.7.10.1
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1214-1224Subventions
Organisme : NIDCR NIH HHS
ID : R01 DE015254
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE024153
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE024716
Pays : United States
Organisme : NIDCR NIH HHS
ID : R37 DE026152
Pays : United States
Informations de copyright
Copyright © 2020 by The American Association of Immunologists, Inc.
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