A loss of tuning of both pro-coagulant and inflammatory responses in monocytes in patients with preeclampsia.

Autor: Nagashima M; Department of Immunology, Yamagata University Faculty of Medicine, Yamagata, Japan; Department of Obstetrics and Gynecology, Yamagata University Faculty of Medicine, Yamagata, Japan., Takeda Y; Department of Immunology, Yamagata University Faculty of Medicine, Yamagata, Japan. Electronic address: yu-takeda@med.id.yamagata-u.ac.jp., Saitoh S; Department of Immunology, Yamagata University Faculty of Medicine, Yamagata, Japan., Sabrina S; Department of Immunology, Yamagata University Faculty of Medicine, Yamagata, Japan., Araki A; Department of Immunology, Yamagata University Faculty of Medicine, Yamagata, Japan., Nagase S; Department of Obstetrics and Gynecology, Yamagata University Faculty of Medicine, Yamagata, Japan., Asao H; Department of Immunology, Yamagata University Faculty of Medicine, Yamagata, Japan.
Jazyk: angličtina
Zdroj: Journal of reproductive immunology [J Reprod Immunol] 2024 Dec; Vol. 166, pp. 104334. Date of Electronic Publication: 2024 Sep 24.
DOI: 10.1016/j.jri.2024.104334
Abstrakt: An imbalance between pro- and anti-angiogenesis is one of the leading causes of preeclampsia (PE). Monocytes, known as regulators of angiogenesis during immune responses, cooperate with platelets, but the specifics of these responses during pregnancy remain unclear. In this study, we investigated the relationship between pro-coagulant responses on monocytes [platelet activation marker CD61 as a monocyte-platelet aggregate (MPA), tissue factor (CD142), etc.], inflammatory responses [soluble CD40 ligand (sCD40L), soluble suppression of tumorigenesis-2 (sST2), etc.], and the balance of angiogenesis [soluble Fms-related receptor tyrosine kinase 1/placental growth factor (sFlt-1/PLGF) ratio]. In PE, markers of pro-coagulant and inflammatory responses were higher than those in normal pregnancy (NP). Interestingly, in NP, these markers harmonized with the sFlt-1/PLGF ratio, but not in PE. Furthermore, ex vivo examinations showed that upregulation of CD142 induced by additional platelet activation with adenosine diphosphate was diminished in PE. Conversely, low-dose aspirin, which is used as a preventive treatment for PE, could inhibit the increase of CD61 and sST2 under inflammatory stimuli and platelet activation in NP but not in PE. These results indicate that monocytes in PE upregulate basal activity and lose responsiveness to stimulation. The elevation of pro-coagulant and inflammatory responses may be mitigated by prophylaxis with low-dose aspirin. Therefore, the findings suggesting a loss of tuning of both pro-coagulant and inflammatory responses on monocytes help in understanding the pathology of PE. The harmonization between pro-coagulant responses, inflammatory responses, and angiogenesis may serve as useful indicators for the prediction and preventive treatment of PE.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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