• 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

大气道中的胶原蛋白沉积可能无法区分重度哮喘与较轻形式的哮喘。

Collagen deposition in large airways may not differentiate severe asthma from milder forms of the disease.

作者信息

Chu H W, Halliday J L, Martin R J, Leung D Y, Szefler S J, Wenzel S E

机构信息

Department of Medicine, National Jewish Medical and Research Center and the University of Colorado Health Sciences Center, Denver, Colorado, USA.

出版信息

Am J Respir Crit Care Med. 1998 Dec;158(6):1936-44. doi: 10.1164/ajrccm.158.6.9712073.

DOI:10.1164/ajrccm.158.6.9712073
PMID:9847289
Abstract

Chronic airway inflammation and remodeling, including fibrosis, have been proposed as important contributors to asthma pathophysiology. Previous studies of airway fibrosis have been performed mainly in mild and moderate asthmatics at the subepithelial "basement membrane" (SBM) level. The current study was designed to evaluate the large airway SBM thickness and submucosal collagen deposition, as measured by three different collagen staining methods, in endobronchial biopsies from 17 severe, nine moderate, and seven mild asthmatics, as well as eight normal control subjects. Tissue eosinophils and transforming growth factor-beta (TGF-beta) immunoreactivity were also examined. There were no statistically significant differences in the SBM thickness, submucosal collagen deposition, eosinophil numbers, or TGF-beta positive cells among the three groups of asthmatics and the normal control subjects. It was only when examining all asthmatics (n = 33) together, that a modestly thickened SBM (p = 0.04), as evaluated by collagen type III immunostaining, was observed as compared with normal control subjects. Despite this difference, no significant differences were found in the amount of submucosal collagen deposition and the number of eosinophils or TGF-beta expressing cells when comparing total asthmatics and normal control subjects. Additionally, no significant correlations were found between collagen deposition and eosinophil count, TGF-beta expression level, FEV1, or duration of asthma. These results suggest that although increased collagen deposition in the SBM at the large airway level is a characteristic of asthma, it may not explain the differences in severity of asthma.

摘要

慢性气道炎症和重塑,包括纤维化,被认为是哮喘病理生理学的重要促成因素。先前关于气道纤维化的研究主要在轻度和中度哮喘患者的上皮下“基底膜”(SBM)水平进行。本研究旨在通过三种不同的胶原染色方法,评估17例重度、9例中度和7例轻度哮喘患者以及8例正常对照受试者的支气管活检中大气道SBM厚度和黏膜下胶原沉积情况。还检测了组织嗜酸性粒细胞和转化生长因子-β(TGF-β)免疫反应性。三组哮喘患者与正常对照受试者在SBM厚度、黏膜下胶原沉积、嗜酸性粒细胞数量或TGF-β阳性细胞方面均无统计学显著差异。仅当将所有哮喘患者(n = 33)一起检查时,与正常对照受试者相比,通过III型胶原免疫染色评估发现SBM有适度增厚(p = 0.04)。尽管存在这种差异,但在比较所有哮喘患者和正常对照受试者时,黏膜下胶原沉积量、嗜酸性粒细胞数量或表达TGF-β的细胞数量均未发现显著差异。此外,在胶原沉积与嗜酸性粒细胞计数、TGF-β表达水平、第一秒用力呼气容积(FEV1)或哮喘病程之间未发现显著相关性。这些结果表明,尽管大气道水平SBM中胶原沉积增加是哮喘的一个特征,但它可能无法解释哮喘严重程度的差异。

相似文献

1
Collagen deposition in large airways may not differentiate severe asthma from milder forms of the disease.大气道中的胶原蛋白沉积可能无法区分重度哮喘与较轻形式的哮喘。
Am J Respir Crit Care Med. 1998 Dec;158(6):1936-44. doi: 10.1164/ajrccm.158.6.9712073.
2
Transforming growth factor-beta expression in mucosal biopsies in asthma and chronic bronchitis.哮喘和慢性支气管炎患者黏膜活检中转化生长因子-β的表达
Am J Respir Crit Care Med. 1997 Aug;156(2 Pt 1):591-9. doi: 10.1164/ajrccm.156.2.9609066.
3
Evidence that severe asthma can be divided pathologically into two inflammatory subtypes with distinct physiologic and clinical characteristics.有证据表明,重度哮喘在病理上可分为两种具有不同生理和临床特征的炎症亚型。
Am J Respir Crit Care Med. 1999 Sep;160(3):1001-8. doi: 10.1164/ajrccm.160.3.9812110.
4
Transforming growth factor beta 1 (TGF beta 1) gene expression by eosinophils in asthmatic airway inflammation.哮喘气道炎症中嗜酸性粒细胞对转化生长因子β1(TGF-β1)基因的表达
Am J Respir Cell Mol Biol. 1996 Sep;15(3):404-9. doi: 10.1165/ajrcmb.15.3.8810646.
5
Bronchial subepithelial fibrosis and expression of matrix metalloproteinase-9 in asthmatic airway inflammation.支气管上皮下纤维化及基质金属蛋白酶-9在哮喘气道炎症中的表达
J Allergy Clin Immunol. 1998 Nov;102(5):783-8. doi: 10.1016/s0091-6749(98)70018-1.
6
Eosinophil-associated TGF-beta1 mRNA expression and airways fibrosis in bronchial asthma.支气管哮喘中嗜酸性粒细胞相关的转化生长因子-β1 mRNA表达与气道纤维化
Am J Respir Cell Mol Biol. 1997 Sep;17(3):326-33. doi: 10.1165/ajrcmb.17.3.2733.
7
Expression of growth factors and remodelling of the airway wall in bronchial asthma.支气管哮喘中生长因子的表达与气道壁重塑
Thorax. 1998 Jan;53(1):21-7. doi: 10.1136/thx.53.1.21.
8
Bronchial responsiveness to distilled water and methacholine and its relationship to inflammation and remodeling of the airways in asthma.支气管对蒸馏水和乙酰甲胆碱的反应性及其与哮喘气道炎症和重塑的关系。
Am J Respir Crit Care Med. 1996 Mar;153(3):910-7. doi: 10.1164/ajrccm.153.3.8630572.
9
Quantitation of mast cells and eosinophils in the bronchial mucosa of symptomatic atopic asthmatics and healthy control subjects using immunohistochemistry.采用免疫组织化学方法对有症状的特应性哮喘患者和健康对照者支气管黏膜中的肥大细胞和嗜酸性粒细胞进行定量分析。
Am Rev Respir Dis. 1990 Oct;142(4):863-71. doi: 10.1164/ajrccm/142.4.863.
10
Vascular endothelial growth factor up-regulation and bronchial wall remodelling in asthma.哮喘中血管内皮生长因子上调与支气管壁重塑
Clin Exp Allergy. 2005 Nov;35(11):1437-42. doi: 10.1111/j.1365-2222.2005.02360.x.

引用本文的文献

1
The Role of Basement Membrane Thickening in Airway Physiology and Immunopathology of Severe Asthma.基底膜增厚在重症哮喘气道生理学和免疫病理学中的作用
Am J Respir Crit Care Med. 2025 Mar 25;211(5):676-7. doi: 10.1164/rccm.202502-0365ED.
2
Increased Muc5AC and Decreased Ciliated Cells in Severe Asthma Partially Restored by Inhibition of IL-4Rα Receptor.严重哮喘中Muc5AC增加和纤毛细胞减少通过抑制IL-4Rα受体得到部分恢复。
Am J Respir Crit Care Med. 2024 Dec 15;210(12):1409-1420. doi: 10.1164/rccm.202307-1266OC.
3
Involvement of Transforming Growth Factor-β-Associated Kinase 1 in Fixed Airway Obstruction in Asthmatic Patients with Longer Disease Duration Independent on Airway Eosinophilia.
转化生长因子-β相关激酶1参与病程较长的哮喘患者的固定性气道阻塞,且与气道嗜酸性粒细胞增多无关。
J Asthma Allergy. 2023 Apr 4;16:343-354. doi: 10.2147/JAA.S403645. eCollection 2023.
4
The Basement Membrane Zone in Asthma: The Supracellular Anchoring Network.哮喘中的基底膜区:超细胞锚定网络。
Curr Respir Med Rev. 2013 Aug;9(4):268-273. doi: 10.2174/1573398x09666131121231852.
5
Mechanical and Physical Regulation of Fibroblast-Myofibroblast Transition: From Cellular Mechanoresponse to Tissue Pathology.成纤维细胞-肌成纤维细胞转分化的机械和物理调节:从细胞力反应到组织病理学
Front Bioeng Biotechnol. 2020 Dec 22;8:609653. doi: 10.3389/fbioe.2020.609653. eCollection 2020.
6
TWIST1 DNA methylation is a cell marker of airway and parenchymal lung fibroblasts that are differentially methylated in asthma.TWIST1 基因启动子区 DNA 甲基化是气道和肺实质成纤维细胞的一种细胞标志物,在哮喘患者中存在差异甲基化。
Clin Epigenetics. 2020 Oct 2;12(1):145. doi: 10.1186/s13148-020-00931-4.
7
Myrcene exerts anti-asthmatic activity in neonatal rats via modulating the matrix remodeling.迷迭香通过调节基质重塑发挥其在新生大鼠中的抗哮喘活性。
Int J Immunopathol Pharmacol. 2020 Jan-Dec;34:2058738420954948. doi: 10.1177/2058738420954948.
8
Airway mechanical compression: its role in asthma pathogenesis and progression.气道机械性压迫:其在哮喘发病机制和进展中的作用。
Eur Respir Rev. 2020 Aug 4;29(157). doi: 10.1183/16000617.0123-2019. Print 2020 Sep 30.
9
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.
10
The Intriguing Role of Interleukin 13 in the Pathophysiology of Asthma.白细胞介素13在哮喘病理生理学中的有趣作用。
Front Pharmacol. 2019 Dec 6;10:1387. doi: 10.3389/fphar.2019.01387. eCollection 2019.