报告时间：2024年08月29日 20:00-21:30
报告人：曹佳雨博士，上海交通交通大学医学院附属仁济医院医师，临床博士后。硕士毕业于上海交通大学医学院，获得外科学硕士学位，后于德国慕尼黑大学获得医学研究哲学博士学位。博士期间研究方向主要是缺血性脑卒中后外周免疫系统调节。博士期间以第一作者身份发表Nature1篇，以共同作者身份发表论文Cell1篇，lmmunity1篇。
主持人：麦鸿成博士，副研究员，博士生导师，中山大学“百人计划”中青年杰出人才。德国慕尼黑大学博士，德国亥姆霍兹国家研究中心博士后。致力于跨器官水平的组织光透明标记与成像技术的研发和应用。曾以第一作者/通讯作者(含共同)于Nature Biotechnology、Nature Protocols、Stroke、Bioactive materials、Advanced Science发表论文，担任VIEW期刊(IF 9.3)，BrainX期刊青年编委会的成员。
文章标题：DNA-sensing inflammasomes cause recurrent atherosclerotic stroke
报告简介
研究摘要
The risk of early recurrent events after stroke remains high despite currently established secondary prevention strategies. Risk is particularly high in patients with atherosclerosis, with more than 10% of patients experiencing early recurrent events. However, despite the enormous medical burden of this clinical phenomenon, the underlying mechanisms leading to increased vascular risk and recurrent stroke are largely unknown. Here, using a novel mouse model of stroke-induced recurrent ischaemia, we show that stroke leads to activation of the AIM2 inflammasome in vulnerable atherosclerotic plaques via an increase of circulating cell-free DNA. Enhanced plaque inflammation post-stroke results in plaque destabilization and atherothrombosis, finally leading to arterioarterial embolism and recurrent stroke within days after the index stroke. We confirm key steps of plaque destabilization also after experimental myocardial infarction and in carotid artery plaque samples from patients with acute stroke. Rapid neutrophil NETosis was identified as the main source of cell-free DNA after stroke and NET–DNA as the causative agent leading to AIM2 inflammasome activation. Neutralization of cell-free DNA by DNase treatment or inhibition of inflammasome activation reduced the rate of stroke recurrence after experimental stroke. Our findings present an explanation for the high recurrence rate after incident ischaemic events in patients with atherosclerosis. The detailed mechanisms uncovered here provide clinically uncharted therapeutic targets for which we show high efficacy to prevent recurrent events. Targeting DNA-mediated inflammasome activation after remote tissue injury represents a promising avenue for further clinical development in the prevention of early recurrent events.
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