Bone morphogenetic protein 9 is a candidate prognostic biomarker and host-directed therapy target for sepsis

生物标志物 体内 败血症 骨形态发生蛋白 细胞因子 吞噬作用 医学 腹膜腔 巨噬细胞 癌症研究 生物 体外 免疫学 基因 免疫系统 解剖 生物技术 生物化学
作者
Haobo Bai,Qian Lu,Chunxiang Wu,Fang Xu,Jiayu Liu,Ke Wang,Hao Ding,Yibing Yin,Yi Liu,Xiaofei Lai,Ju Cao
出处
期刊:Science Translational Medicine [American Association for the Advancement of Science]
卷期号:16 (732): eadi3275-eadi3275 被引量:27
标识
DOI:10.1126/scitranslmed.adi3275
摘要

Defining next-generation immune therapeutics for the treatment of sepsis will involve biomarker-based therapeutic decision-making. Bone morphogenetic protein 9 (BMP9) is a cytokine in the transforming growth factor-β superfamily. Here, circulating BMP9 concentrations were quantified in two independent cohorts of patients with sepsis. Decreased concentrations of serum BMP9 were observed in the patients with sepsis at the time of admission as compared with healthy controls. Concentrations of BMP9 at the time of admission were also associated with 28-day mortality, because patients with sepsis at a higher risk of death had lower BMP9 concentrations. The mechanism driving the contribution of BMP9 to host immunity was further investigated using in vivo murine sepsis models and in vitro cell models. We found that BMP9 treatment improved outcome in mice with experimental sepsis. BMP9-treated mice exhibited increased macrophage influx into the peritoneal cavity and more efficient bacterial clearance than untreated mice. In vitro, BMP9 promoted macrophage recruitment, phagocytosis, and subsequent bacterial killing. We further found that deletion of the type 1 BMP receptor ALK1 in macrophages abolished BMP9-mediated protection against polymicrobial sepsis in vivo. Further experiments indicated that the regulation of macrophage activation by the BMP9-ALK1 axis was mainly mediated through the suppressor of mother against decapentaplegic 1/5 signaling pathway. Together, these results suggest that BMP9 can both serve as a biomarker for patient stratification with an independent prognostic value and be developed as a host-directed therapy for sepsis.
最长约 10秒,即可获得该文献文件

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
高大的羿完成签到,获得积分10
刚刚
jiangjiarui发布了新的文献求助10
刚刚
枓妍通管家完成签到,获得积分10
刚刚
刚刚
shmily发布了新的文献求助10
刚刚
细心傲南发布了新的文献求助10
1秒前
rico完成签到,获得积分10
1秒前
夏硕发布了新的文献求助10
1秒前
youli完成签到 ,获得积分10
2秒前
2秒前
2秒前
orixero应助南风采纳,获得10
3秒前
zyyzyyoo完成签到,获得积分10
3秒前
huhu完成签到,获得积分10
4秒前
爆米花应助奋斗朋友采纳,获得10
4秒前
CipherSage应助可靠的怜南采纳,获得10
4秒前
Mansis完成签到,获得积分10
4秒前
Skye完成签到,获得积分10
4秒前
4秒前
4秒前
SLab完成签到,获得积分10
5秒前
5秒前
jostar26发布了新的文献求助10
5秒前
陈佩chenpei发布了新的文献求助10
6秒前
7秒前
maodonky发布了新的文献求助10
7秒前
小马甲应助简单尔风采纳,获得10
7秒前
科研通AI6.4应助change采纳,获得10
8秒前
sailingray发布了新的文献求助10
8秒前
科研通AI6.4应助哇owao采纳,获得10
9秒前
9秒前
象征江湖发布了新的文献求助10
10秒前
demon1完成签到,获得积分10
10秒前
fx发布了新的文献求助10
10秒前
星星发布了新的文献求助10
10秒前
zzz完成签到,获得积分10
11秒前
maver发布了新的文献求助10
11秒前
打打应助闫晓美采纳,获得10
11秒前
11秒前
11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
Resistance Spot Welding Dataset for Automobile Body-in-White Quality Analysis 748
日本現代怪異事典 副読本 700
悉尼大学博士学位论文,题目:Modelling and testing of one-sided stitched laminated composites. 作者:Kristopher P. Plain 650
Machine Learning for Asset Management and Pricing 600
Numerical analysis of the coupled atmosphere-ocean models (CAO II). II 600
Models for the coupled atmosphere and ocean 600
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7387941
求助须知:如何正确求助?哪些是违规求助? 8994426
关于积分的说明 19138212
捐赠科研通 7024605
什么是DOI,文献DOI怎么找? 3228214
关于科研通互助平台的介绍 2390785
邀请新用户注册赠送积分活动 2209310