• 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

桦树花粉的低分子量成分对支气管上皮屏障完整性的调节作用。

Modulation of Bronchial Epithelial Barrier Integrity by Low Molecular Weight Components from Birch Pollen.

机构信息

Department of Dermatology, University Hospital Sankt Poelten, Karl Landsteiner University of Health Sciences, 3100 Sankt Poelten, Austria.

Institute of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, 1090 Vienna, Austria.

出版信息

Int J Mol Sci. 2024 Jul 5;25(13):7374. doi: 10.3390/ijms25137374.

DOI:10.3390/ijms25137374
PMID:39000481
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11242533/
Abstract

Pollen, in addition to allergens, comprise low molecular weight components (LMC) smaller than 3 kDa. Emerging evidence indicates the relevance of LMC in allergic immune responses. However, the interaction of birch pollen (BP)-derived LMC and epithelial cells has not been extensively studied. We investigated epithelial barrier modifications induced by exposure to BP LMC, using the human bronchial epithelial cell line 16HBE14o-. Epithelial cell monolayers were apically exposed to the major BP allergen Bet v 1, aqueous BP extract or BP-derived LMC. Barrier integrity after the treatments was monitored by measuring transepithelial electrical resistance at regular intervals and by using the xCELLigence Real-Time Cell Analysis system. The polarized release of cytokines 24 h following treatment was measured using a multiplex immunoassay. Epithelial barrier integrity was significantly enhanced upon exposure to BP LMC. Moreover, BP LMC induced the repair of papain-mediated epithelial barrier damage. The apical release of CCL5 and TNF-α was significantly reduced after exposure to BP LMC, while the basolateral release of IL-6 significantly increased. In conclusion, the results of our study demonstrate that BP-derived LMC modify the physical and immunological properties of bronchial epithelial cells and thus regulate airway epithelial barrier responses.

摘要

花粉除过敏原外,还包括小于 3 kDa 的低分子量成分 (LMC)。新出现的证据表明 LMC 在过敏免疫反应中的相关性。然而,桦树花粉 (BP) 衍生的 LMC 与上皮细胞的相互作用尚未得到广泛研究。我们使用人支气管上皮细胞系 16HBE14o-研究了暴露于 BP LMC 后上皮细胞屏障的改变。上皮细胞单层被 BP 的主要过敏原 Bet v 1、水提 BP 提取物或 BP 衍生的 LMC 经顶侧处理。通过定期测量跨上皮电阻和使用 xCELLigence 实时细胞分析系统来监测处理后的屏障完整性。使用多重免疫分析测量处理后 24 小时细胞因子的极化释放。暴露于 BP LMC 后,上皮屏障完整性显著增强。此外,BP LMC 诱导了木瓜蛋白酶介导的上皮屏障损伤的修复。暴露于 BP LMC 后,CCL5 和 TNF-α 的顶端释放明显减少,而 IL-6 的基底外侧释放明显增加。总之,我们的研究结果表明,BP 衍生的 LMC 改变了支气管上皮细胞的物理和免疫特性,从而调节气道上皮屏障反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c80/11242533/4d11145beef7/ijms-25-07374-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c80/11242533/89556fcb7a05/ijms-25-07374-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c80/11242533/ca51ef5b8d0e/ijms-25-07374-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c80/11242533/4d11145beef7/ijms-25-07374-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c80/11242533/89556fcb7a05/ijms-25-07374-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c80/11242533/ca51ef5b8d0e/ijms-25-07374-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c80/11242533/4d11145beef7/ijms-25-07374-g003.jpg

相似文献

1
Modulation of Bronchial Epithelial Barrier Integrity by Low Molecular Weight Components from Birch Pollen.桦树花粉的低分子量成分对支气管上皮屏障完整性的调节作用。
Int J Mol Sci. 2024 Jul 5;25(13):7374. doi: 10.3390/ijms25137374.
2
Fish-derived low molecular weight components modify bronchial epithelial barrier properties and release of pro-inflammatory cytokines.鱼类来源的低分子量成分可改变支气管上皮屏障功能并释放促炎细胞因子。
Mol Immunol. 2019 Aug;112:140-150. doi: 10.1016/j.molimm.2019.04.029. Epub 2019 May 15.
3
IFN-gamma-enhanced allergen penetration across respiratory epithelium augments allergic inflammation.γ干扰素增强变应原穿过呼吸道上皮的能力,从而加剧变应性炎症。
J Allergy Clin Immunol. 2005 May;115(5):973-81. doi: 10.1016/j.jaci.2005.01.021.
4
Direct contact between dendritic cells and bronchial epithelial cells inhibits T cell recall responses towards mite and pollen allergen extracts in vitro.树突状细胞与支气管上皮细胞之间的直接接触在体外抑制了T细胞对螨和花粉过敏原提取物的回忆反应。
Clin Exp Immunol. 2015 Aug;181(2):207-18. doi: 10.1111/cei.12611. Epub 2015 Jun 11.
5
Barrier responses of human bronchial epithelial cells to grass pollen exposure.人支气管上皮细胞对草花粉暴露的屏障反应。
Eur Respir J. 2013 Jul;42(1):87-97. doi: 10.1183/09031936.00075612. Epub 2012 Nov 8.
6
The major birch pollen allergen Bet v 1 induces different responses in dendritic cells of birch pollen allergic and healthy individuals.主要桦树花粉过敏原 Bet v 1 可诱导桦树花粉过敏和健康个体树突状细胞产生不同的反应。
PLoS One. 2015 Jan 30;10(1):e0117904. doi: 10.1371/journal.pone.0117904. eCollection 2015.
7
TNF-α-mediated bronchial barrier disruption and regulation by src-family kinase activation.TNF-α 介导致支气管屏障破坏及 src 家族激酶激活的调控。
J Allergy Clin Immunol. 2013 Sep;132(3):665-675.e8. doi: 10.1016/j.jaci.2013.03.005. Epub 2013 Apr 28.
8
Cigarette smoke-induced disruption of bronchial epithelial tight junctions is prevented by transforming growth factor-β.香烟烟雾引起的支气管上皮紧密连接破坏可被转化生长因子-β所阻止。
Am J Respir Cell Mol Biol. 2014 Jun;50(6):1040-52. doi: 10.1165/rcmb.2013-0090OC.
9
Kinetics, cross-reactivity, and specificity of Bet v 1-specific IgG4 antibodies induced by immunotherapy with birch pollen.免疫治疗桦树花粉引起的 Bet v 1 特异性 IgG4 抗体的动力学、交叉反应性和特异性。
Allergy. 2013 Nov;68(11):1377-86. doi: 10.1111/all.12236. Epub 2013 Sep 21.
10
Reactions of airway epithelial cells to birch pollen grains previously exposed to in situ atmospheric Pb concentrations: a preliminary assay of allergenicity.气道上皮细胞对先前暴露于原位大气 Pb 浓度下的桦树花粉粒的反应:变应原性的初步测定。
Biol Trace Elem Res. 2012 Dec;150(1-3):391-5. doi: 10.1007/s12011-012-9485-7. Epub 2012 Aug 16.

引用本文的文献

1
Modeling Human Airway Epithelial Barrier Penetration Using Birch Bet v 1 and Alder Aln g 1 Pollen Allergens During Sensitization Process.在致敏过程中使用桦树花粉过敏原Bet v 1和桤木花粉过敏原Aln g 1模拟人类气道上皮屏障穿透
Int J Mol Sci. 2025 May 28;26(11):5169. doi: 10.3390/ijms26115169.

本文引用的文献

1
The History and Science of the Major Birch Pollen Allergen Bet v 1.主要桦树花粉过敏原 Bet v 1 的历史和科学。
Biomolecules. 2023 Jul 19;13(7):1151. doi: 10.3390/biom13071151.
2
EAACI Molecular Allergology User's Guide 2.0.欧洲变态反应和临床免疫学会分子变态反应学用户指南2.0
Pediatr Allergy Immunol. 2023 Mar;34 Suppl 28:e13854. doi: 10.1111/pai.13854.
3
Patterns of Phenolic Compounds in and Pollen.[植物名称]和花粉中酚类化合物的模式
Plants (Basel). 2023 Jan 12;12(2):356. doi: 10.3390/plants12020356.
4
How Do Pollen Allergens Sensitize?花粉过敏原是如何致敏的?
Front Mol Biosci. 2022 Jun 16;9:900533. doi: 10.3389/fmolb.2022.900533. eCollection 2022.
5
Initiating pollen sensitization - complex source, complex mechanisms.引发花粉致敏——来源复杂,机制复杂。
Clin Transl Allergy. 2020 Aug 31;10:36. doi: 10.1186/s13601-020-00341-y. eCollection 2020.
6
The role of eosinophils in chronic spontaneous urticaria.嗜酸性粒细胞在慢性自发性荨麻疹中的作用。
J Allergy Clin Immunol. 2020 Jun;145(6):1510-1516. doi: 10.1016/j.jaci.2020.03.005. Epub 2020 Mar 26.
7
Lipid Mediators From Timothy Grass Pollen Contribute to the Effector Phase of Allergy and Prime Dendritic Cells for Glycolipid Presentation. Timothy 草花粉中的脂质介质有助于过敏的效应期,并为糖脂呈递致敏树突状细胞。
Front Immunol. 2019 May 7;10:974. doi: 10.3389/fimmu.2019.00974. eCollection 2019.
8
Fish-derived low molecular weight components modify bronchial epithelial barrier properties and release of pro-inflammatory cytokines.鱼类来源的低分子量成分可改变支气管上皮屏障功能并释放促炎细胞因子。
Mol Immunol. 2019 Aug;112:140-150. doi: 10.1016/j.molimm.2019.04.029. Epub 2019 May 15.
9
IL-9 promotes the pathogenesis of ulcerative colitis through STAT3/SOCS3 signaling.白细胞介素-9 通过 STAT3/SOCS3 信号促进溃疡性结肠炎的发病机制。
Biosci Rep. 2018 Nov 28;38(6). doi: 10.1042/BSR20181521. Print 2018 Dec 21.
10
The probiotic strain Escherichia coli Nissle 1917 prevents papain-induced respiratory barrier injury and severe allergic inflammation in mice.益生菌菌株大肠杆菌 Nissle 1917 可预防木瓜蛋白酶诱导的小鼠呼吸屏障损伤和严重过敏炎症。
Sci Rep. 2018 Jul 26;8(1):11245. doi: 10.1038/s41598-018-29689-9.