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妊娠激素混合物对未激活和 LPS 激活的 THP-1 分化的单核细胞/巨噬细胞细胞因子产生和表面标志物表达的影响。

Effect of pregnancy hormone mixtures on cytokine production and surface marker expression in naïve and LPS-activated THP-1 differentiated monocytes/macrophages.

机构信息

Departamento de Fisiología, Universidad de Guadalajara, Centro Universitario de Ciencias de la Salud, Mexico.

Universidad de Guadalajara, Centro Universitario de Ciencias de la Salud, Instituto de Investigación en Reumatología y Sistema Músculo-Esquelético, Mexico.

出版信息

Innate Immun. 2020 Feb;26(2):84-96. doi: 10.1177/1753425919864658. Epub 2019 Jul 31.

DOI:10.1177/1753425919864658
PMID:31364430
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7016408/
Abstract

In pregnancy, maternal monocytes and macrophages acquire a specific phenotype that enables them to maintain immune tolerance and facilitate hormone–immune cell interactions, which are necessary for gestational progression. The aim of this study was to determine the effect of pregnancy hormone mixtures of the first and third trimesters on both resting and activated monocytes and macrophages. Pregnancy hormone levels (cortisol, estradiol, progesterone, and prolactin) were quantified at the first and third trimesters. The average of the levels obtained was used to prepare two mixtures of synthetic hormones: low and high. These mixtures were then used to stimulate THP-1 monocytes and macrophages, resting or activated with LPS. Cytokine production in the culture supernatants and surface marker expression (CD14, CD86, and CD163) were evaluated by ELISA and flow cytometry, respectively. We found that the hormones modulated the pro-inflammatory response of THP-1 cells, LPS-activated monocytes, and macrophages, inducing high levels of IL-10 and low levels of IL-8, IL-1-β, and IL-6. All hormone stimulation increased the CD163 receptor in both resting and LPS-activated monocytes and macrophages in a dose-independent manner, unlike CD14 and CD86. Pregnancy hormones promote the expression of the markers associated with the M2-like phenotype, modulating their pro-inflammatory response. This phenotype regulation by hormones could be a determinant in pregnancy.

摘要

在妊娠期间,母体单核细胞和巨噬细胞获得特定的表型,使其能够维持免疫耐受并促进激素-免疫细胞相互作用,这对于妊娠进展是必要的。本研究旨在确定妊娠第一和第三 trimester 的激素混合物对静止和激活的单核细胞和巨噬细胞的影响。在第一和第三 trimester 量化了妊娠激素水平(皮质醇、雌二醇、孕酮和催乳素)。使用获得的水平的平均值来制备两种合成激素混合物:低和高。然后使用这些混合物刺激 THP-1 单核细胞和巨噬细胞,用 LPS 或 LPS 激活。通过 ELISA 和流式细胞术分别评估培养上清液中的细胞因子产生和表面标志物表达(CD14、CD86 和 CD163)。我们发现,激素调节了 THP-1 细胞、LPS 激活的单核细胞和巨噬细胞的促炎反应,诱导高水平的 IL-10 和低水平的 IL-8、IL-1-β 和 IL-6。所有激素刺激均以剂量非依赖性方式增加了静止和 LPS 激活的单核细胞和巨噬细胞中 CD163 受体的表达,而 CD14 和 CD86 则不然。妊娠激素促进与 M2 样表型相关的标志物的表达,调节其促炎反应。这种由激素调节的表型可能是妊娠的决定因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9407/7016408/04e75dea4fea/10.1177_1753425919864658-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9407/7016408/e5898838a3cf/10.1177_1753425919864658-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9407/7016408/91001f338281/10.1177_1753425919864658-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9407/7016408/836c843caaad/10.1177_1753425919864658-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9407/7016408/04e75dea4fea/10.1177_1753425919864658-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9407/7016408/e5898838a3cf/10.1177_1753425919864658-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9407/7016408/91001f338281/10.1177_1753425919864658-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9407/7016408/836c843caaad/10.1177_1753425919864658-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9407/7016408/04e75dea4fea/10.1177_1753425919864658-fig4.jpg

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