• 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

变应性哮喘患者变应原激发5分钟后支气管肺泡灌洗液介质水平:与迟发性哮喘反应发生的关系

Bronchoalveolar lavage fluid mediator levels 5 minutes after allergen challenge in atopic subjects with asthma: relationship to the development of late asthmatic responses.

作者信息

Wenzel S E, Westcott J Y, Larsen G L

机构信息

Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colo. 80206.

出版信息

J Allergy Clin Immunol. 1991 Feb;87(2):540-8. doi: 10.1016/0091-6749(91)90013-e.

DOI:10.1016/0091-6749(91)90013-e
PMID:1993813
Abstract

Inflammatory mediators have been implicated in the pathogenesis of human asthma and have been demonstrated to increase in bronchoalveolar lavage fluid during the time of the immediate asthmatic response (IAR) after allergen instillation in the lungs. However, the relationship of these mediators, measured early to the late asthmatic response (LAR), airway reactivity, and clinical asthma, is unknown. In the present study, we evaluated mediator levels in bronchoalveolar lavage fluid before and 5 minutes after allergen challenge from three subject groups: atopic subjects without asthma (N = 7), atopic subjects with asthma and without LAR [-) LAR) (N = 6), and atopic subjects with asthma and with LAR [+) LAR) (N = 6). Subjects with asthma were differentiated into subjects with and without LARs based on at least a 15% decrease in FEV1 between 3 to 8 hours postallergen inhalation. The mediators, prostaglandin D2 thromboxane B2 leukotriene C4 (LTC4), and histamine, were measured both before and after allergen instillation. Baseline prechallenge levels were similar, except in the case of LTC4. LTC4 was detectable at baseline significantly more frequently in the atopic subjects with asthma with and without LAR when these subjects were compared to the atopic subjects without asthma (nine of 12 detectable versus one of seven detectable). In all groups, significant increases in mediator levels were observed in the groups with asthma postallergen challenge, compared to the atopic subjects without asthma. Atopic subjects with asthma and without LAR had significantly higher levels of all four mediators after challenge than atopic subjects with asthma and with LAR and atopic subjects without asthma.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

炎症介质与人类哮喘的发病机制有关,并且已证实在肺部吸入变应原后即刻哮喘反应(IAR)期间,支气管肺泡灌洗液中的炎症介质会增加。然而,这些早期测量的介质与迟发性哮喘反应(LAR)、气道反应性和临床哮喘之间的关系尚不清楚。在本研究中,我们评估了三组受试者在变应原激发前和激发后5分钟支气管肺泡灌洗液中的介质水平:无哮喘的特应性受试者(N = 7)、无LAR的哮喘特应性受试者[-) LAR](N = 6)和有LAR的哮喘特应性受试者[+) LAR](N = 6)。根据变应原吸入后3至8小时内FEV1至少下降15%,将哮喘受试者分为有LAR和无LAR的受试者。在变应原注入前后均测量了前列腺素D2、血栓素B2、白三烯C4(LTC4)和组胺等介质。除LTC4外,激发前的基线水平相似。与无哮喘的特应性受试者相比,有LAR和无LAR的哮喘特应性受试者在基线时LTC4的可检测频率显著更高(12例中有9例可检测到,而7例中有1例可检测到)。与无哮喘的特应性受试者相比,所有哮喘组在变应原激发后介质水平均显著升高。无LAR的哮喘特应性受试者在激发后所有四种介质的水平均显著高于有LAR的哮喘特应性受试者和无哮喘的特应性受试者。(摘要截短于250字)

相似文献

1
Bronchoalveolar lavage fluid mediator levels 5 minutes after allergen challenge in atopic subjects with asthma: relationship to the development of late asthmatic responses.变应性哮喘患者变应原激发5分钟后支气管肺泡灌洗液介质水平:与迟发性哮喘反应发生的关系
J Allergy Clin Immunol. 1991 Feb;87(2):540-8. doi: 10.1016/0091-6749(91)90013-e.
2
Elevated levels of leukotriene C4 in bronchoalveolar lavage fluid from atopic asthmatics after endobronchial allergen challenge.支气管内过敏原激发后,特应性哮喘患者支气管肺泡灌洗液中白三烯C4水平升高。
Am Rev Respir Dis. 1990 Jul;142(1):112-9. doi: 10.1164/ajrccm/142.1.112.
3
Histamine release from bronchoalveolar lavage cells from asthmatic subjects after allergen challenge and relationship to the late asthmatic response.变应原激发后哮喘患者支气管肺泡灌洗细胞的组胺释放及其与哮喘迟发反应的关系。
Clin Exp Allergy. 1998 Feb;28(2):196-204. doi: 10.1046/j.1365-2222.1998.00228.x.
4
Spectrum of prostanoid release after bronchoalveolar allergen challenge in atopic asthmatics and in control groups. An alteration in the ratio of bronchoconstrictive to bronchoprotective mediators.特应性哮喘患者和对照组在支气管肺泡过敏原激发后类前列腺素释放谱。支气管收缩介质与支气管保护介质比例的改变。
Am Rev Respir Dis. 1989 Feb;139(2):450-7. doi: 10.1164/ajrccm/139.2.450.
5
Activation of pulmonary mast cells by bronchoalveolar allergen challenge. In vivo release of histamine and tryptase in atopic subjects with and without asthma.支气管肺泡变应原激发对肺肥大细胞的激活作用。组胺和类胰蛋白酶在有或无哮喘的特应性受试者体内的释放情况。
Am Rev Respir Dis. 1988 May;137(5):1002-8. doi: 10.1164/ajrccm/137.5.1002.
6
The inhibitory effect of terfenadine and flurbiprofen on early and late-phase bronchoconstriction following allergen challenge in atopic asthma.特非那定和氟比洛芬对特应性哮喘患者变应原激发后早发和迟发性支气管收缩的抑制作用。
Clin Exp Allergy. 1990 May;20(3):261-7. doi: 10.1111/j.1365-2222.1990.tb02681.x.
7
Effect of a leukotriene B4 receptor antagonist, LY293111, on allergen induced responses in asthma.白三烯B4受体拮抗剂LY293111对哮喘变应原诱导反应的影响。
Thorax. 1996 Dec;51(12):1178-84. doi: 10.1136/thx.51.12.1178.
8
Allergen-induced airway reactions in atopic asthmatics correlate with allergen-specific IL-5 response by BAL cells.变应性哮喘患者中变应原诱导的气道反应与支气管肺泡灌洗(BAL)细胞的变应原特异性白细胞介素-5反应相关。
Respirology. 1997 Mar;2(1):45-55. doi: 10.1111/j.1440-1843.1997.tb00053.x.
9
Inflammatory cells and eicosanoid mediators in subjects with late asthmatic responses and increases in airway responsiveness.迟发性哮喘反应和气道反应性增加患者中的炎症细胞和类花生酸介质。
J Allergy Clin Immunol. 1992 Jun;89(6):1076-84. doi: 10.1016/0091-6749(92)90291-9.
10
Increased secretion of tumor necrosis factor alpha and interleukin-6 by alveolar macrophages consecutive to the development of the late asthmatic reaction.
J Allergy Clin Immunol. 1991 Oct;88(4):561-71. doi: 10.1016/0091-6749(91)90149-i.

引用本文的文献

1
Pathobiology and Regulation of Eosinophils, Mast Cells, and Basophils in Allergic Asthma.过敏性哮喘中嗜酸性粒细胞、肥大细胞和嗜碱性粒细胞的病理生物学与调控
Immunol Rev. 2025 May;331(1):e70018. doi: 10.1111/imr.70018.
2
Pulmonary Eosinophils at the Center of the Allergic Space-Time Continuum.过敏性时空中的中心:肺部嗜酸性粒细胞。
Front Immunol. 2021 Nov 15;12:772004. doi: 10.3389/fimmu.2021.772004. eCollection 2021.
3
Novel Strategies to Target Mast Cells in Disease.靶向疾病中肥大细胞的新策略。
J Innate Immun. 2021;13(3):131-147. doi: 10.1159/000513582. Epub 2021 Feb 12.
4
G Protein-Coupled Receptors in Asthma Therapy: Pharmacology and Drug Action.哮喘治疗中的 G 蛋白偶联受体:药理学和药物作用。
Pharmacol Rev. 2020 Jan;72(1):1-49. doi: 10.1124/pr.118.016899.
5
The prostaglandin D receptor 2 pathway in asthma: a key player in airway inflammation.哮喘中的前列腺素 D 受体 2 途径:气道炎症的关键因素。
Respir Res. 2018 Sep 29;19(1):189. doi: 10.1186/s12931-018-0893-x.
6
COX-1 mediates IL-33-induced extracellular signal-regulated kinase activation in mast cells: Implications for aspirin sensitivity.COX-1 介导白介素-33 诱导的肥大细胞细胞外信号调节激酶激活:对阿司匹林敏感性的影响。
J Allergy Clin Immunol. 2019 Mar;143(3):1047-1057.e8. doi: 10.1016/j.jaci.2018.06.033. Epub 2018 Jul 12.
7
Expression and Activity of COX-1 and COX-2 in Acanthamoeba sp.-Infected Lungs According to the Host Immunological Status.根据宿主免疫状态,探讨 CoX-1 和 COX-2 在棘阿米巴属感染肺组织中的表达和活性。
Int J Mol Sci. 2018 Jan 2;19(1):121. doi: 10.3390/ijms19010121.
8
Regulation of Eosinophil and Group 2 Innate Lymphoid Cell Trafficking in Asthma.哮喘中嗜酸性粒细胞和2型固有淋巴细胞转运的调控
Front Med (Lausanne). 2017 Aug 11;4:136. doi: 10.3389/fmed.2017.00136. eCollection 2017.
9
Allergic asthma is distinguished by sensitivity of allergen-specific CD4+ T cells and airway structural cells to type 2 inflammation.过敏性哮喘的特征是过敏原特异性CD4+ T细胞和气道结构细胞对2型炎症敏感。
Sci Transl Med. 2016 Oct 5;8(359):359ra132. doi: 10.1126/scitranslmed.aag1370.
10
Aspirin-Exacerbated Respiratory Disease Involves a Cysteinyl Leukotriene-Driven IL-33-Mediated Mast Cell Activation Pathway.阿司匹林加重性呼吸疾病涉及半胱氨酰白三烯驱动的白细胞介素-33介导的肥大细胞激活途径。
J Immunol. 2015 Oct 15;195(8):3537-45. doi: 10.4049/jimmunol.1500905. Epub 2015 Sep 4.