A large-scale single-cell atlas reveals the pulmonary immune panorama in adult patients with influenza

免疫系统 免疫学 医学 免疫病理学 细胞激素风暴 支气管肺泡灌洗 细胞因子 疾病 获得性免疫系统 先天免疫系统 流式细胞术 免疫失调 炎症 细胞免疫 呼吸道疾病 中性粒细胞胞外陷阱 病理 生物 肺泡蛋白沉积症 免疫功能障碍 甲型流感病毒 重症监护
作者
Kun Xiao,Y B Cao,Zhihai Han,Qian Da,Yi Feng,Rong Tian,Laurence Don Wai Luu,Li Zhang,Xiaoyan Li,Ruijuan Wang,Xiang Li,Mei Hu,Fucheng An,Xiangxin Li,Fei Zhang,Shubin Qiao,Qingrong Nie,Ping Jiang,Xia Ma,Ye Hu
出处
期刊:American Journal of Respiratory and Critical Care Medicine [American Thoracic Society]
卷期号:212 (7): 1548-1568
标识
DOI:10.1093/ajrccm/aamag122
摘要

RATIONALE: The host immune determinants that distinguish protective from life-threatening responses to influenza are poorly understood. Identifying drivers of immunopathology in the human lung is critical for developing potential therapies. OBJECTIVES: To define the cellular and molecular immune landscape of the lung in mild vs severe influenza and to identify key cellular states and pathways associated with disease severity. METHODS: We generated a large-scale single-cell atlas by sequencing more than 520 000 cells from the bronchoalveolar lavage fluid of 88 nonimmunocompromised adult individuals with mild or severe influenza A and healthy controls. Key findings were validated by flow cytometry and protein quantification, and machine-learning models were used to identify predictive signatures. MAIN RESULTS: Severe influenza was characterized by profound pulmonary lymphopenia and a massive influx of functionally dysregulated neutrophils. The infiltrating neutrophils were primed for extracellular trap formation, driving a cytokine storm via the S100A8/A9/A12-TLR4 and CXCL8-CXCR1/2 axes. This pathology coincided with the depletion and functional impairment of resident alveolar macrophages and an expansion of pro-inflammatory, monocyte-derived macrophages that amplified neutrophil recruitment. Lymphopenia in severe disease arose from synergistic cell-death programs, while remaining lymphocytes exhibited a dysfunctional state of concurrent exhaustion and hypercytotoxicity. Mild influenza featured a coordinated adaptive immune response, distinguished by an enrichment of T follicular helper cells and plasma cells. Machine-learning models identified robust cellular and transcriptional signatures predictive of disease severity. CONCLUSIONS: Our atlas defines the divergent immune trajectories in influenza, revealing specific cellular states and pathways that drive immunopathology and provide novel targets for host-directed therapies.
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
冷HorToo完成签到 ,获得积分10
刚刚
Watson完成签到,获得积分10
刚刚
Orange应助科研通管家采纳,获得10
1秒前
cdercder应助科研通管家采纳,获得10
1秒前
1秒前
高大的向南完成签到,获得积分10
2秒前
2秒前
义气天真完成签到,获得积分10
2秒前
小马甲应助科研通管家采纳,获得10
2秒前
真实的芝完成签到,获得积分20
2秒前
缥缈的幻雪完成签到 ,获得积分10
2秒前
科目三应助科研通管家采纳,获得10
2秒前
senquana完成签到,获得积分10
2秒前
2秒前
科研通AI2S应助科研通管家采纳,获得10
2秒前
汉堡包应助科研通管家采纳,获得10
2秒前
riccixuu完成签到 ,获得积分10
2秒前
传奇3应助科研通管家采纳,获得10
2秒前
asder完成签到,获得积分10
3秒前
酷波er应助科研通管家采纳,获得10
3秒前
3秒前
小北完成签到,获得积分10
3秒前
左左蕊发布了新的文献求助10
3秒前
3秒前
3秒前
在水一方应助kkk采纳,获得10
3秒前
3秒前
科研通AI6.4应助zwk采纳,获得10
3秒前
3秒前
3秒前
烟花应助崔晴晴采纳,获得10
3秒前
3秒前
深情安青应助xiuwenli采纳,获得10
3秒前
3秒前
陈严完成签到,获得积分10
3秒前
charles完成签到 ,获得积分10
4秒前
Lena完成签到,获得积分10
5秒前
bibi完成签到,获得积分10
5秒前
温暖万天完成签到,获得积分10
5秒前
zhengke924完成签到,获得积分10
6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
Römisch-Germanische Forschungen 1000
Social Psychology (第二版) 700
China Pluperfect I: Epistemology of Past and Outside in Chinese Art 520
Matrix Methods in Data Mining and Pattern Recognition Second Edition 510
The fast track to determining transfer functions of linear circuits: The student guide 500
The Analytical and Numerical Solution of Electric and Magnetic Fields 500
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 7613475
求助须知:如何正确求助?哪些是违规求助? 9188846
关于积分的说明 19686248
捐赠科研通 7186523
什么是DOI,文献DOI怎么找? 3270850
关于科研通互助平台的介绍 2434402
邀请新用户注册赠送积分活动 2265801