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oai:repisalud.isciii.es:20.500.12105/66662024-09-27T09:11:49Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Salinas-Munoz, Laura author Campos-Fernandez, Raul author Mercader, Enrique author Olivera-Valle, Irene author Fernandez-Pacheco, Carlota author Matilla, Lara author Garcia-Bordas, Julio author Brazil, Jennifer C. author Parkos, Charles A. author Asensio, Fernando author Munoz-Fernandez, Maria A. author Hidalgo, Andres author Sanchez-Mateos, Paloma author Samaniego, Rafael author Relloso, Miguel author 2018 Estradiol-based therapies predispose women to vaginal infections. Moreover, it has long been known that neutrophils are absent from the vaginal lumen during the ovulatory phase (high estradiol). However, the mechanisms that regulate neutrophil influx to the vagina remain unknown. We investigated the neutrophil transepithelial migration (TEM) into the vaginal lumen. We revealed that estradiol reduces the CD44 and CD47 epithelial expression in the vaginal ectocervix and fornix, which retain neutrophils at the apical epithelium through the estradiol receptor-alpha. In contrast, luteal progesterone increases epithelial expression of CD44 and CD47 to promote neutrophil migration into the vaginal lumen and Candida albicans destruction. Distinctive to vaginal mucosa, neutrophil infiltration is contingent to sex hormones to prevent sperm from neutrophil attack; although it may compromise immunity during ovulation. Thus, sex hormones orchestrate tolerance and immunity in the vaginal lumen by regulating neutrophil TEM. Front Immunol. 2018; 9:1033 10.3389/fimmu.2018.01033 1664-3224 Frontiers in Immunology 29881378 http://hdl.handle.net/20.500.12105/6666 Estradiol ESR1 Progesterone Neutrophils Transepithelial migration Cervix NEUTROPHIL-EPITHELIAL INTERACTIONS TRANSEPITHELIAL MIGRATION SEX-HORMONES INTESTINAL EPITHELIUM CHEMOKINE GRADIENTS VAGINA TRANSMIGRATION IMMUNITY CELLS INFILTRATION Estrogen Receptor-Alpha (ESR1) Governs the Lower Female Reproductive Tract Vulnerability to Candida albicans