• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

鼻腔上皮与巨噬细胞和树突状细胞的相互作用可改变健康人群、哮喘和 COPD 患者对城市 PM 诱导的炎症反应。

Interactions of nasal epithelium with macrophages and dendritic cells variously alter urban PM-induced inflammation in healthy, asthma and COPD.

机构信息

Department of Internal Medicine, Pulmonary Diseases and Allergy, Medical University of Warsaw, Banacha 1a, 02-097, Warsaw, Poland.

Postgraduate School of Molecular Medicine, Medical University of Warsaw, Warsaw, Poland.

出版信息

Sci Rep. 2021 Jun 24;11(1):13259. doi: 10.1038/s41598-021-92626-w.

DOI:10.1038/s41598-021-92626-w
PMID:34168212
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8225888/
Abstract

Urban particulate matter (UPM) is an important trigger of airway inflammation. The cross-talk between the external and internal matrix in the respiratory tract occurs due to the transepithelial network of macrophages/dendritic cells. This study characterized the immune processes induced by the epithelium after UPM exposure in special regard to interactions with monocyte-derived dendritic cells (moDCs) and monocyte-derived macrophages (moMφs) in obstructive lung diseases. A triple-cell co-culture model (8 controls, 10 asthma, and 8 patients with COPD) utilized nasal epithelial cells, along with moMφs, and moDCs was exposed to UPM for 24 h. The inflammatory response of nasal epithelial cells to UPM stimulation is affected differently by cell-cell interactions in healthy people, asthma or COPD patients of which the interactions with DCs had the strongest impact on the inflammatory reaction of epithelial cells after UPM exposure. The epithelial remodeling and DCs dysfunction might accelerate the inflammation after air pollution exposure in asthma and COPD.

摘要

城市颗粒物 (UPM) 是气道炎症的重要触发因素。由于呼吸道内的巨噬细胞/树突状细胞的跨上皮网络，外部和内部基质之间发生串扰。本研究特别针对阻塞性肺疾病中与单核细胞衍生的树突状细胞 (moDC) 和单核细胞衍生的巨噬细胞 (moMφ) 的相互作用，描述了 UPM 暴露后上皮细胞诱导的免疫过程。三重细胞共培养模型（8 个对照、10 个哮喘和 8 个 COPD 患者）利用鼻上皮细胞，以及 moMφ 和 moDC，暴露于 UPM 24 小时。鼻上皮细胞对 UPM 刺激的炎症反应在健康人、哮喘或 COPD 患者中受到细胞间相互作用的不同影响，其中与 DC 的相互作用对 UPM 暴露后上皮细胞的炎症反应有最强的影响。上皮重塑和 DC 功能障碍可能会加速哮喘和 COPD 患者在空气污染暴露后的炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/2c1145048479/41598_2021_92626_Fig14_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/983efb8dc3fa/41598_2021_92626_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/556b5d9a73a3/41598_2021_92626_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/3660dac4c648/41598_2021_92626_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/c1c169554578/41598_2021_92626_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/1a61d5ae89a9/41598_2021_92626_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/80bf11b1da10/41598_2021_92626_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/4c5d772728ed/41598_2021_92626_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/b8f6270add48/41598_2021_92626_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/05f69b87fc8e/41598_2021_92626_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/b9a580a9b154/41598_2021_92626_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/7face2cc00bb/41598_2021_92626_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/90084543ba74/41598_2021_92626_Fig12_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/9631659bec21/41598_2021_92626_Fig13_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/2c1145048479/41598_2021_92626_Fig14_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/983efb8dc3fa/41598_2021_92626_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/556b5d9a73a3/41598_2021_92626_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/3660dac4c648/41598_2021_92626_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/c1c169554578/41598_2021_92626_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/1a61d5ae89a9/41598_2021_92626_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/80bf11b1da10/41598_2021_92626_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/4c5d772728ed/41598_2021_92626_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/b8f6270add48/41598_2021_92626_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/05f69b87fc8e/41598_2021_92626_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/b9a580a9b154/41598_2021_92626_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/7face2cc00bb/41598_2021_92626_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/90084543ba74/41598_2021_92626_Fig12_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/9631659bec21/41598_2021_92626_Fig13_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0190/8225888/2c1145048479/41598_2021_92626_Fig14_HTML.jpg

相似文献

1
Interactions of nasal epithelium with macrophages and dendritic cells variously alter urban PM-induced inflammation in healthy, asthma and COPD.鼻腔上皮与巨噬细胞和树突状细胞的相互作用可改变健康人群、哮喘和 COPD 患者对城市 PM 诱导的炎症反应。
Sci Rep. 2021 Jun 24;11(1):13259. doi: 10.1038/s41598-021-92626-w.
2
The Expressions of TSLP, IL-33, and IL-17A in Monocyte Derived Dendritic Cells from Asthma and COPD Patients are Related to Epithelial-Macrophage Interactions.哮喘和 COPD 患者来源的树突状细胞中 TSLP、IL-33 和 IL-17A 的表达与上皮-巨噬细胞相互作用有关。
Cells. 2020 Aug 22;9(9):1944. doi: 10.3390/cells9091944.
3
RNA-Seq Analysis of UPM-Exposed Epithelium Co-Cultivated with Macrophages and Dendritic Cells in Obstructive Lung Diseases.UPM 暴露的上皮细胞与巨噬细胞和树突状细胞共培养在阻塞性肺疾病中的 RNA-Seq 分析。
Int J Mol Sci. 2022 Aug 15;23(16):9125. doi: 10.3390/ijms23169125.
4
Urban Particulate Matter-Activated Human Dendritic Cells Induce the Expansion of Potent Inflammatory Th1, Th2, and Th17 Effector Cells.城市颗粒物激活的人树突状细胞诱导强效炎性Th1、Th2和Th17效应细胞扩增。
Am J Respir Cell Mol Biol. 2016 Feb;54(2):250-62. doi: 10.1165/rcmb.2015-0084OC.
5
Epithelial-macrophage-dendritic cell interactions impact alarmins expression in asthma and COPD.上皮细胞-巨噬细胞-树突状细胞相互作用影响哮喘和 COPD 中警报素的表达。
Clin Immunol. 2020 Jun;215:108421. doi: 10.1016/j.clim.2020.108421. Epub 2020 Apr 14.
6
Urban particulate matter stimulation of human dendritic cells enhances priming of naive CD8 T lymphocytes.城市颗粒物刺激人树突状细胞增强幼稚 CD8 T 淋巴细胞的启动。
Immunology. 2018 Apr;153(4):502-512. doi: 10.1111/imm.12852. Epub 2017 Nov 28.
7
Effects of fetal exposure to urban particulate matter on the immune system of male mouse offspring.胎儿暴露于城市颗粒物对雄性小鼠后代免疫系统的影响。
Biol Pharm Bull. 2012;35(8):1238-43. doi: 10.1248/bpb.b110708.
8
Tumor necrosis factor-α mediates interactions between macrophages and epithelial cells underlying proinflammatory gene expression induced by particulate matter.肿瘤坏死因子-α介导颗粒物诱导的促炎基因表达中巨噬细胞和上皮细胞之间的相互作用。
Toxicology. 2012 Sep 28;299(2-3):125-32. doi: 10.1016/j.tox.2012.05.014. Epub 2012 May 23.
9
Urban particulate matter suppresses priming of T helper type 1 cells by granulocyte/macrophage colony-stimulating factor-activated human dendritic cells.城市颗粒物通过粒细胞/巨噬细胞集落刺激因子激活的人树突状细胞抑制 T 辅助细胞 1 型细胞的启动。
Am J Respir Cell Mol Biol. 2014 Feb;50(2):281-91. doi: 10.1165/rcmb.2012-0465OC.
10
Genome-Wide Analysis Reveals Mucociliary Remodeling of the Nasal Airway Epithelium Induced by Urban PM.全基因组分析揭示城市 PM 诱导的鼻腔气道上皮纤毛重塑
Am J Respir Cell Mol Biol. 2020 Aug;63(2):172-184. doi: 10.1165/rcmb.2019-0454OC.

引用本文的文献

1
Exploring the pathogenesis and clinical implications of asthma, chronic obstructive pulmonary disease (COPD), and asthma-COPD overlap (ACO): a narrative review.探索哮喘、慢性阻塞性肺疾病（COPD）及哮喘-慢性阻塞性肺疾病重叠综合征（ACO）的发病机制及临床意义：一项叙述性综述
Front Med (Lausanne). 2025 Apr 17;12:1514846. doi: 10.3389/fmed.2025.1514846. eCollection 2025.
2
models to study viral-induced asthma exacerbation: a short review for a key issue.用于研究病毒诱导的哮喘加重的模型：一个关键问题的简短综述
Front Allergy. 2025 Mar 28;6:1530122. doi: 10.3389/falgy.2025.1530122. eCollection 2025.
3
Frequency of Exacerbations of Chronic Obstructive Pulmonary Disease Associated with the Long-Term Exposure to Air Pollution in the AIREPOC Cohort.

本文引用的文献

1
Titanium dioxide particles modulate epithelial barrier protein, Claudin 7 in asthma.二氧化钛颗粒可调节哮喘中的上皮屏障蛋白 Claudin 7。
Mol Immunol. 2021 Apr;132:209-216. doi: 10.1016/j.molimm.2021.01.004. Epub 2021 Jan 19.
2
Airway-Associated Macrophages in Homeostasis and Repair.气道相关巨噬细胞在稳态和修复中的作用。
Cell Rep. 2020 Dec 29;33(13):108553. doi: 10.1016/j.celrep.2020.108553.
3
Potential role of polycyclic aromatic hydrocarbons in air pollution-induced non-malignant respiratory diseases.多环芳烃在空气污染引起的非恶性呼吸道疾病中的潜在作用。
AIREPOC队列中与长期暴露于空气污染相关的慢性阻塞性肺疾病急性加重频率
Int J Chron Obstruct Pulmon Dis. 2025 Feb 22;20:425-435. doi: 10.2147/COPD.S498437. eCollection 2025.
4
The impaired response of nasal epithelial cells to microplastic stimulation in asthma and COPD.哮喘和慢性阻塞性肺疾病中鼻上皮细胞对微塑料刺激的反应受损。
Sci Rep. 2025 Feb 4;15(1):4242. doi: 10.1038/s41598-025-87242-x.
5
Nasal Mucociliary Epithelial Cell Culture Models for Studying Viral Infections.用于研究病毒感染的鼻黏膜纤毛上皮细胞培养模型
Methods Mol Biol. 2025;2890:237-252. doi: 10.1007/978-1-0716-4326-6_13.
6
Link between respiratory microbiota and asthma: an emerging therapeutic approach.呼吸道微生物群与哮喘之间的联系：一种新兴的治疗方法。
Am J Transl Res. 2024 Nov 15;16(11):6289-6302. doi: 10.62347/OSNZ1705. eCollection 2024.
7
The effect of air pollutants on COPD-hospitalized patients in Lanzhou, China (2015-2019).中国兰州地区空气污染物对 COPD 住院患者的影响（2015-2019 年）。
Front Public Health. 2024 Sep 19;12:1399662. doi: 10.3389/fpubh.2024.1399662. eCollection 2024.
8
The Relationship between Fine Particle Matter (PM2.5) Exposure and Upper Respiratory Tract Diseases.细颗粒物（PM2.5）暴露与上呼吸道疾病之间的关系。
J Pers Med. 2024 Jan 16;14(1):98. doi: 10.3390/jpm14010098.
9
On the path to predicting immune responses in the lung: Modeling the pulmonary innate immune system at the air-liquid interface (ALI).在预测肺部免疫反应的道路上：在气液界面（ALI）模拟肺部先天免疫系统。
Eur J Pharm Sci. 2023 Dec 1;191:106596. doi: 10.1016/j.ejps.2023.106596. Epub 2023 Sep 26.
10
Macrophages Orchestrate Airway Inflammation, Remodeling, and Resolution in Asthma.巨噬细胞在哮喘中调控气道炎症、重塑和修复。
Int J Mol Sci. 2023 Jun 21;24(13):10451. doi: 10.3390/ijms241310451.
Respir Res. 2020 Nov 13;21(1):299. doi: 10.1186/s12931-020-01563-1.
4
Epithelial-interleukin-1 inhibits collagen formation by airway fibroblasts: Implications for asthma.上皮细胞-白细胞介素-1 抑制气道成纤维细胞胶原形成：对哮喘的影响。
Sci Rep. 2020 May 26;10(1):8721. doi: 10.1038/s41598-020-65567-z.
5
Respiratory exposure to PM2.5 soluble extract disrupts mucosal barrier function and promotes the development of experimental asthma.呼吸暴露于 PM2.5 可溶提取物会破坏黏膜屏障功能并促进实验性哮喘的发展。
Sci Total Environ. 2020 Aug 15;730:139145. doi: 10.1016/j.scitotenv.2020.139145. Epub 2020 May 3.
6
Particulate Matter Decreases Intestinal Barrier-Associated Proteins Levels in 3D Human Intestinal Model.颗粒物降低 3D 人肠道模型中肠道屏障相关蛋白水平。
Int J Environ Res Public Health. 2020 May 6;17(9):3234. doi: 10.3390/ijerph17093234.
7
Epithelial-macrophage-dendritic cell interactions impact alarmins expression in asthma and COPD.上皮细胞-巨噬细胞-树突状细胞相互作用影响哮喘和 COPD 中警报素的表达。
Clin Immunol. 2020 Jun;215:108421. doi: 10.1016/j.clim.2020.108421. Epub 2020 Apr 14.
8
Genome-Wide Analysis Reveals Mucociliary Remodeling of the Nasal Airway Epithelium Induced by Urban PM.全基因组分析揭示城市 PM 诱导的鼻腔气道上皮纤毛重塑
Am J Respir Cell Mol Biol. 2020 Aug;63(2):172-184. doi: 10.1165/rcmb.2019-0454OC.
9
Localization of Macrophages in the Human Lung via Design-based Stereology.基于设计的体视学方法定位人肺中的巨噬细胞。
Am J Respir Crit Care Med. 2020 May 15;201(10):1209-1217. doi: 10.1164/rccm.201911-2105OC.
10
Modifiers of the effect of short-term variation in PM on mortality in Beijing, China.中国北京短期 PM 变化对死亡率影响的修饰因子。
Environ Res. 2020 Apr;183:109066. doi: 10.1016/j.envres.2019.109066. Epub 2019 Dec 26.