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获得性主动脉瓣狭窄患者中免疫球蛋白E网络成分与主动脉瓣面积相关。

Elements of Immunoglobulin E Network Associate with Aortic valve Area in Patients with Acquired Aortic Stenosis.

作者信息

Potaczek Daniel P, Przytulska-Szczerbik Aleksandra, Bazan-Socha Stanisława, Jurczyszyn Artur, Okumura Ko, Nishiyama Chiharu, Undas Anetta, Wypasek Ewa

机构信息

Translational Inflammation Research Division & Core Facility for Single Cell Multiomics, Medical Faculty, Philipps University Marburg, Member of the German Center for Lung Research (DZL) and the Universities of Giessen and Marburg Lung Center, 35043 Marburg, Germany.

Krakow Center for Medical Research and Technology, John Paul II Hospital, 31-202 Krakow, Poland.

出版信息

Biomedicines. 2020 Dec 31;9(1):23. doi: 10.3390/biomedicines9010023.

DOI:10.3390/biomedicines9010023
PMID:33396395
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7824289/
Abstract

Allergic mechanisms are likely involved in atherosclerosis and its clinical presentations, such as coronary artery disease (CAD). It has been previously reported that CAD severity associates with serum levels of immunoglobulin E (IgE), the molecule that, along with its high-affinity receptor (FcԑRI), plays a central role in allergic reactions. Considering multiple pathophysiological similarities between atherosclerosis and acquired aortic (valve) stenosis (AS), we speculated that allergic pathways could also contribute to the AS mechanisms and grading. To validate this hypothesis, we first checked whether total serum IgE levels associate with echocardiographic markers of AS severity. Having found a positive correlation between serum IgE and aortic valve area (AVA), we further speculated that also total IgE-determining genetic polymorphisms in , a locus encoding an allergen-biding FcԑRI subunit, are related to acquired AS severity. Indeed, the major allele of rs2251746 polymorphism, known to associate with higher IgE levels, turned out to correlate with larger AVA, a marker of less severe AS. Our findings surprisingly suggest a protective role of IgE pathways against AS progression. IgE-mediated protective mechanisms in AS require further investigations.

摘要

过敏机制可能参与动脉粥样硬化及其临床表现,如冠状动脉疾病(CAD)。此前有报道称,CAD的严重程度与免疫球蛋白E(IgE)的血清水平相关,IgE分子与其高亲和力受体(FcԑRI)在过敏反应中起核心作用。考虑到动脉粥样硬化与后天性主动脉(瓣膜)狭窄(AS)之间存在多种病理生理相似性,我们推测过敏途径也可能参与AS的发病机制和分级。为了验证这一假设,我们首先检查了血清总IgE水平是否与AS严重程度的超声心动图指标相关。发现血清IgE与主动脉瓣面积(AVA)呈正相关后,我们进一步推测,编码过敏原结合FcԑRI亚基的基因座中的总IgE决定基因多态性也与后天性AS的严重程度有关。事实上,已知与较高IgE水平相关的rs2251746多态性的主要等位基因,结果与较大的AVA相关,AVA是AS较轻的一个指标。我们的研究结果令人惊讶地表明,IgE途径对AS进展具有保护作用。IgE介导的AS保护机制需要进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a83/7824289/df0f3a02f99a/biomedicines-09-00023-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a83/7824289/96891d2793e0/biomedicines-09-00023-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a83/7824289/17dcc807dbf5/biomedicines-09-00023-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a83/7824289/df0f3a02f99a/biomedicines-09-00023-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a83/7824289/96891d2793e0/biomedicines-09-00023-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a83/7824289/17dcc807dbf5/biomedicines-09-00023-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a83/7824289/df0f3a02f99a/biomedicines-09-00023-g003.jpg

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