Estradiol suppresses psoriatic inflammation in mice by regulating neutrophil and macrophage functions.
Estradiol
IL-17A
IL-1β
estrogen receptor
macrophage
neutrophil
psoriasis
Journal
The Journal of allergy and clinical immunology
ISSN: 1097-6825
Titre abrégé: J Allergy Clin Immunol
Pays: United States
ID NLM: 1275002
Informations de publication
Date de publication:
10 2022
10 2022
Historique:
received:
24
08
2021
revised:
21
02
2022
accepted:
18
03
2022
pubmed:
20
5
2022
medline:
12
10
2022
entrez:
19
5
2022
Statut:
ppublish
Résumé
Psoriasis is a common inflammatory skin disease resulting from dysregulation of the IL-23/T We studied whether estradiol, a female hormone, plays protective roles in imiquimod-induced psoriatic inflammation in mice by regulating neutrophil and macrophage functions. Wild-type mice and conditional knockout mice were ovariectomized, supplemented with placebo or estradiol pellets, and an imiquimod-containing cream applied. Mice without endogenous ovarian hormones exhibited exacerbated psoriatic inflammation including increased production of IL-17A and IL-1β, which was reversed by exogenously added estradiol. The suppressive effect of estradiol on the production of IL-1β and IL-17A was abolished in mice lacking estrogen receptors in neutrophils and macrophages (Esr1 Our results suggest a novel mechanism for sex-dependent differences in psoriasis clinical phenotypes that may shed new light on the pathology of psoriasis.
Sections du résumé
BACKGROUND
Psoriasis is a common inflammatory skin disease resulting from dysregulation of the IL-23/T
OBJECTIVE
We studied whether estradiol, a female hormone, plays protective roles in imiquimod-induced psoriatic inflammation in mice by regulating neutrophil and macrophage functions.
METHODS
Wild-type mice and conditional knockout mice were ovariectomized, supplemented with placebo or estradiol pellets, and an imiquimod-containing cream applied.
RESULTS
Mice without endogenous ovarian hormones exhibited exacerbated psoriatic inflammation including increased production of IL-17A and IL-1β, which was reversed by exogenously added estradiol. The suppressive effect of estradiol on the production of IL-1β and IL-17A was abolished in mice lacking estrogen receptors in neutrophils and macrophages (Esr1
CONCLUSION
Our results suggest a novel mechanism for sex-dependent differences in psoriasis clinical phenotypes that may shed new light on the pathology of psoriasis.
Identifiants
pubmed: 35589416
pii: S0091-6749(22)00485-7
doi: 10.1016/j.jaci.2022.03.028
pii:
doi:
Substances chimiques
Interleukin-17
0
Interleukin-23
0
Receptors, Estrogen
0
Estradiol
4TI98Z838E
Imiquimod
P1QW714R7M
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
909-919.e8Informations de copyright
Copyright © 2022 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.