figshare
Browse
GOI_201607025_1_11_Supplementary_figure.pdf (77.52 kB)

Supplementary Material for: Decidualization Mediated by Steroid Hormones Modulates the Innate Immunity in Response to Group B Streptococcal Infection in vitro

Download (77.52 kB)
figure
posted on 2017-02-01, 12:42 authored by Castro-Leyva V., Zaga-Clavellina V., Espejel-Nuñez A., Vega-Sanchez R., Flores-Pliego A., Reyes-Muñoz E., Giono-Cerezo S., Nava-Salazar S., Espino y Sosa S., Estrada-Gutierrez G.

Background: Decidual cells play a role in the modulation of the innate immune response to protect pregnancy against infection. Steroid hormones regulate the innate immune response in different tissues, and they are involved in several biological processes like decidualization. The aim of this study was to assess if steroid hormones modulate the innate immunity in endometrial stromal cells (ESCs) and decidual stromal cells (DSCs) in response to group B streptococcus (GBS) infection in vitro. Methods: Primary cultures of ESC were differentiated into DSC using 36 nM estradiol + 300 nM progesterone, and both were infected with GBS overnight. Concentrations of pro- and anti-inflammatory mediators (interleukin [IL]-1β, IL-6, tumor necrosis factor [TNF]-α, IL-10, and TGF-β), chemokines (IL-8 and GCP-2), and human β-defensins (HBD-1, HBD-2, and HBD-3) were measured in the culture supernatants. Results: DSCs showed a significant increase in IL-6 (p < 0.05), TNF-α (p < 0.05), IL-10 (p < 0.01), and TGF-β (p < 0.05) secretion after GBS infection, while these changes were not observed in infected ESCs. IL-8 and GCP-2 increased after GBS infection, regardless of decidualization. β-Defensins 1-3 decreased (p < 0.05) in ESCs after GBS infection, and hormone decidualization preserved the secretion of these antimicrobial peptides. Conclusions: Decidualization mediated by steroid hormones balance the pro- and anti-inflammatory response at the maternal-fetal interface under infection conditions.

History

Usage metrics

    Gynecologic and Obstetric Investigation

    Categories

    Licence

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC