The interplay of Cxcl10+/Mmp14+ monocytes and Ccl3+ neutrophils proactively mediates silica-induced pulmonary fibrosis

矽肺 肺纤维化 纤维化 化学 CXCL10型 单核细胞 趋化因子 免疫学 医学 炎症 病理 内科学
作者
Demin Cheng,Wenxiu Lian,Ting Wang,Sichuan Xi,Xinying Jia,Ziwei Li,Haojie Xiong,Yue Wang,Wenqing Sun,Siyun Zhou,Peng Lan,Lei Han,Yi Liu,Chunhui Ni
出处
期刊:Journal of Hazardous Materials [Elsevier BV]
卷期号:467: 133713-133713 被引量:6
标识
DOI:10.1016/j.jhazmat.2024.133713
摘要

As a fatal occupational disease with limited therapeutic options, molecular mechanisms underpinning silicosis are still undefined. Herein, single-cell RNA sequencing of the lung tissue of silicosis mice identified two monocyte subsets, which were characterized by Cxcl10 and Mmp14 and enriched in fibrotic mouse lungs. Both Cxcl10+ and Mmp14+ monocyte subsets exhibited activation of inflammatory marker genes and positive regulation of cytokine production. Another fibrosis-unique neutrophil population characterized by Ccl3 appeared to be related to the pro-fibrotic process, specifically the "inflammatory response". Meanwhile, the proportion of monocytes and neutrophils was significantly higher in the serum of silicosis patients and slices of lung tissue from patients with silicosis further validated the over-expression of Cxcl10 and Mmp14 in monocytes, also Ccl3 in neutrophils, respectively. Mechanically, receptor-ligand interaction analysis identified the crosstalk of Cxcl10+/Mmp14+ monocytes with Ccl3+ neutrophils promoting fibrogenesis via coupling of HBEGF-CD44 and CSF1-CSF1R. In vivo, administration of clodronate liposomes, Cxcl10 or Mmp14 siRNA-loaded liposomes, Ccl3 receptor antagonist BX471, CD44 or CSF1R neutralizing antibodies significantly alleviated silica-induced lung fibrosis. Collectively, these results demonstrate that the newly defined Cxcl10+/Mmp14+ monocytes and Ccl3+ neutrophils participate in the silicosis process and highlight anti-receptor-ligand pair treatment as a potentially effective therapeutic strategy in managing silicosis.
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
JamesPei应助无限的幼萱采纳,获得10
刚刚
1秒前
宋心茹关注了科研通微信公众号
1秒前
Mea发布了新的文献求助10
2秒前
3秒前
大虫子发布了新的文献求助10
4秒前
wanci应助独特的自中采纳,获得10
5秒前
江峰发布了新的文献求助10
6秒前
紫陌完成签到,获得积分10
6秒前
YPP发布了新的文献求助30
7秒前
zhangyue7777完成签到,获得积分10
7秒前
crane发布了新的文献求助30
7秒前
8秒前
8秒前
科研通AI5应助笑面客采纳,获得10
9秒前
lojack完成签到,获得积分10
10秒前
fdffff完成签到,获得积分20
10秒前
11秒前
11秒前
frost发布了新的文献求助10
12秒前
宗语雪完成签到,获得积分10
12秒前
14秒前
浅言完成签到 ,获得积分10
14秒前
orange9发布了新的文献求助10
14秒前
15秒前
书晗完成签到,获得积分20
15秒前
思源应助江峰采纳,获得10
15秒前
迷你的颖发布了新的文献求助10
16秒前
16秒前
小乐比完成签到,获得积分10
17秒前
17秒前
17秒前
酱紫应助叁壹捌采纳,获得10
18秒前
19秒前
Tse发布了新的文献求助10
20秒前
20秒前
21秒前
星空完成签到,获得积分10
21秒前
花生完成签到 ,获得积分10
21秒前
SciGPT应助liu采纳,获得10
22秒前
高分求助中
【此为提示信息,请勿应助】请按要求发布求助,避免被关 20000
Continuum Thermodynamics and Material Modelling 2000
105th Edition CRC Handbook of Chemistry and Physics 1600
ISCN 2024 – An International System for Human Cytogenomic Nomenclature (2024) 1000
CRC Handbook of Chemistry and Physics 104th edition 1000
Izeltabart tapatansine - AdisInsight 600
Maneuvering of a Damaged Navy Combatant 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 物理 生物化学 纳米技术 计算机科学 化学工程 内科学 复合材料 物理化学 电极 遗传学 量子力学 基因 冶金 催化作用
热门帖子
关注 科研通微信公众号,转发送积分 3769817
求助须知:如何正确求助?哪些是违规求助? 3314838
关于积分的说明 10173969
捐赠科研通 3030157
什么是DOI,文献DOI怎么找? 1662662
邀请新用户注册赠送积分活动 795062
科研通“疑难数据库(出版商)”最低求助积分说明 756539