Evaluation of endometrial immune status of polycystic ovary syndrome

多囊卵巢 超重 医学 内科学 子宫内膜 免疫系统 人口 川地68 体质指数 内分泌学 胰岛素抵抗 妇科 肥胖 免疫学 免疫组织化学 环境卫生
作者
Su Liu,Hong Li,Meilan Mo,Shan Xiao,Cong Chen,Yuye Li,Ruochun Lian,Xuejin Wang,Songchen Cai,Lianghui Diao,Yong Zeng
出处
期刊:Journal of Reproductive Immunology [Elsevier BV]
卷期号:144: 103282-103282 被引量:16
标识
DOI:10.1016/j.jri.2021.103282
摘要

Polycystic ovary syndrome (PCOS) is described as a low-grade chronic inflammatory state. However, there are limited studies on the specific endometrial immune status of PCOS patients. Whether this endometrial immune cell pattern is intrinsic to PCOS or the consequence of PCOS-associated obesity is a subject of debate. This study retrospectively included one hundred women diagnosed with PCOS and ninety-five normal fertile controls, which further divided into four groups (normoweight PCOS; overweight PCOS; normoweight control; overweight control) based on body mass index. The percentages of endometrial CD68+ macrophages (1.97 % vs. 1.17 %; P < 0.001), CD163+ M2 macrophages (2.30 % vs. 1.83 %; P = 0.001), CD1a+ iDCs (0.044 % vs. 0.029 %; P = 0.002), CD83+ mDCs (1.72 % vs. 1.07 %; P < 0.001) and CD8+ T cells (2.82 % vs. 1.95 %; P < 0.001) were significantly higher in normoweight PCOS women than normoweight controls. The percentage of CD68+ macrophages (2.09 % vs. 1.15 %; P < 0.001) was significantly higher in overweight PCOS women compared with overweight controls. In multivariant linear regression analysis, participants' PCOS status was the main predictors of endometrial CD68+ macrophages, CD163+ M2 macrophages, CD1a+ iDCs, CD83+ mDCs and CD8+ T cells in the whole study population. Additionally, in PCOS group, positive correlations were found between endometrial CD56+ NK, CD163+ M2 macrophages and QUICKI, indicating there was an association between endometrial immune cells and insulin resistance in PCOS women. Our study suggests that women with PCOS have altered endometrial immune cells, which may reflect a state of chronic low grade inflammation. The chronic inflammation, independent of obesity, may help understand the pathophysiologic mechanisms of intrinsic PCOS.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
负责惊蛰完成签到,获得积分10
刚刚
NexusExplorer应助allen采纳,获得10
刚刚
Morgan发布了新的文献求助10
1秒前
JamesPei应助sunrise采纳,获得10
1秒前
孤影完成签到,获得积分10
2秒前
bkagyin应助不加糖采纳,获得10
2秒前
2秒前
li完成签到 ,获得积分10
3秒前
4秒前
4秒前
大模型应助Felix0917采纳,获得10
5秒前
王三石完成签到,获得积分10
6秒前
8秒前
李李李发布了新的文献求助10
8秒前
Garvey完成签到,获得积分10
8秒前
8秒前
困困包发布了新的文献求助10
9秒前
9秒前
9秒前
独特亦旋发布了新的文献求助10
10秒前
张铭发布了新的文献求助10
11秒前
13秒前
13秒前
allen发布了新的文献求助10
13秒前
大模型应助安静海云采纳,获得10
14秒前
墨尔根戴青完成签到,获得积分10
14秒前
Jrssion发布了新的文献求助10
14秒前
一二发布了新的文献求助10
15秒前
王硕完成签到,获得积分10
15秒前
小鱼完成签到,获得积分10
16秒前
李爱国应助li074采纳,获得10
16秒前
Mr兔仙森发布了新的文献求助10
16秒前
科研通AI6.3应助李李李采纳,获得10
16秒前
灰太狼大王完成签到 ,获得积分10
18秒前
嗯qq发布了新的文献求助10
18秒前
doctorsu发布了新的文献求助10
20秒前
缓慢逍遥完成签到 ,获得积分10
21秒前
敏玥发布了新的文献求助10
23秒前
ice_cream发布了新的文献求助10
23秒前
25秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Modern Epidemiology, Fourth Edition 5000
Handbook of pharmaceutical excipients, Ninth edition 5000
Digital Twins of Advanced Materials Processing 2000
Weaponeering, Fourth Edition – Two Volume SET 2000
Polymorphism and polytypism in crystals 1000
Signals, Systems, and Signal Processing 610
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 纳米技术 有机化学 生物化学 化学工程 物理 计算机科学 复合材料 内科学 催化作用 物理化学 光电子学 电极 冶金 基因 遗传学
热门帖子
关注 科研通微信公众号,转发送积分 6023090
求助须知:如何正确求助?哪些是违规求助? 7646777
关于积分的说明 16171357
捐赠科研通 5171450
什么是DOI,文献DOI怎么找? 2767125
邀请新用户注册赠送积分活动 1750492
关于科研通互助平台的介绍 1637045