Estradiol impairs epithelial CXCL1 gradient in the cervix to delay neutrophil transepithelial migration during insemination.
Animals
Cervix Uteri
/ cytology
Chemokine CXCL1
/ metabolism
Estradiol
/ metabolism
Estrogen Receptor alpha
/ genetics
Female
Immune Tolerance
Insemination
/ immunology
Male
Mice
Mice, Knockout
Mucous Membrane
/ immunology
Neutrophils
/ immunology
Spermatozoa
/ immunology
Transendothelial and Transepithelial Migration
/ immunology
Cervix
ESR1
Estradiol
Neutrophils
Progesterone
Sperm
Journal
Journal of reproductive immunology
ISSN: 1872-7603
Titre abrégé: J Reprod Immunol
Pays: Ireland
ID NLM: 8001906
Informations de publication
Date de publication:
04 2019
04 2019
Historique:
received:
29
10
2018
revised:
24
01
2019
accepted:
17
02
2019
pubmed:
27
2
2019
medline:
9
6
2020
entrez:
27
2
2019
Statut:
ppublish
Résumé
Female reproductive mucosa must allow allogenic sperm survival whereas at the same time, avoid pathogen infection. To preserve sperm from neutrophil attack, neutrophils disappear from the vagina during the ovulatory phase (high estradiol); although the mechanisms that regulate neutrophil influx to the vagina during insemination remain controversial. We investigated the sex hormone regulation of the neutrophil migration through the cervix during insemination and revealed that ovulatory estradiol dose fades the CXCL1 epithelial expression in the ectocervix and fornix; hence, retarding neutrophil migration and retaining them in the epithelium. These mechanisms spare sperm from neutrophil attack to preserve reproduction, but might compromise immunity. However, luteal progesterone dose promotes the CXCL1 gradient expression to restore neutrophil migration, to eliminate sperm and prevent sperm associated pathogen dissemination. Surprisingly, these mechanisms are hormone dependent and independent of the insemination. Thus, sex hormones orchestrate tolerance and immunity in the vaginal lumen by regulating neutrophil transepithelial migration in the fornix and ectocervix.
Identifiants
pubmed: 30807979
pii: S0165-0378(18)30334-6
doi: 10.1016/j.jri.2019.02.002
pii:
doi:
Substances chimiques
Chemokine CXCL1
0
Cxcl1 protein, mouse
0
Esr1 protein, mouse
0
Estrogen Receptor alpha
0
Estradiol
4TI98Z838E
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
9-15Informations de copyright
Copyright © 2019 Elsevier B.V. All rights reserved.