Influence of menopause status on T-helper cell profiles in acute myocardial infarction.

0 MEDICINE, RESEARCH & EXPERIMENTAL
Fernanda Espinosa-Bautista, Varna Ramos-Rosillo, Yadira V Ázquez-Panchos, Fernanda Bocanegra-Zamora, Héctor González-Pacheco, Mariana Patlán, Araceli Páez, Felipe Massó, Luis M Amezcua-Guerra
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Abstract

Estrogens modulate immune responses, particularly the activation and polarization of CD4+ T cells, which play key roles in cardiovascular homeostasis. This proof-of-concept study investigated the effect of menopausal status on the polarization of T-helper (Th) cells in women with acute myocardial infarction (AMI). A total of 41 female AMI patients were enrolled-seven premenopausal and 34 postmenopausal-and compared with a group of 17 male AMI patients. Flow cytometry was used to evaluate CD4+ T-cell subsets, including Th1 (T-bet+), Th2 (GATA3+), and Th17 (RORγt+) phenotypes. Serum levels of representative cytokines were also measured. Women exhibited higher numbers of circulating CD4+ T cells compared to men, with a marked shift toward the Th1 phenotype. Postmenopausal women demonstrated increased cardiovascular risk, as indicated by higher QRISK3 and GRACE scores, as well as elevated levels of C-reactive protein and cardiac troponin T compared to premenopausal women. However, menopausal status had minimal impact on Th cell polarization, as no significant differences were observed in the proportions of Th1, Th2, or Th17 subsets between premenopausal and postmenopausal women. Similarly, levels of interleukin (IL)-6, IL-1β, IL-10, tumor necrosis factor, and monocyte chemoattractant protein-1 were comparable between the two groups. This proof-of-concept study highlights sex-specific differences in immune responses and inflammatory profiles during AMI. Women exhibited a stronger polarization toward the Th1 phenotype, along with elevated markers of inflammation and myocardial injury. Notably, menopausal status did not significantly affect lymphocyte subpopulations or circulating cytokine levels.

绝经状态对急性心肌梗死患者t辅助细胞谱的影响。
雌激素调节免疫反应,特别是CD4+ T细胞的激活和极化,在心血管稳态中起关键作用。这项概念验证性研究调查了绝经状态对急性心肌梗死(AMI)妇女t辅助细胞(Th)极化的影响。共有41名女性AMI患者(7名绝经前患者和34名绝经后患者)被纳入研究,并与一组17名男性AMI患者进行比较。流式细胞术检测CD4+ t细胞亚群,包括Th1 (T-bet+)、Th2 (GATA3+)和Th17 (RORγt+)表型。血清中代表性细胞因子的水平也被测量。与男性相比,女性表现出更多的循环CD4+ T细胞,并明显转向Th1表型。与绝经前妇女相比,绝经后妇女表现出心血管风险增加,如更高的QRISK3和GRACE评分,以及c反应蛋白和心肌肌钙蛋白T水平升高。然而,绝经状态对Th细胞极化的影响很小,因为绝经前和绝经后妇女在Th1、Th2或Th17亚群的比例上没有观察到显著差异。同样,白细胞介素(IL)-6、IL-1β、IL-10、肿瘤坏死因子和单核细胞化学引诱蛋白-1的水平在两组之间具有可比性。这项概念验证研究强调了AMI期间免疫反应和炎症特征的性别特异性差异。女性表现出更强的Th1表型极化,同时炎症和心肌损伤标志物升高。值得注意的是,绝经状态对淋巴细胞亚群或循环细胞因子水平没有显著影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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CiteScore
1.10
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