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1
Reproducibility of a novel model of murine asthma-like pulmonary inflammation.一种新型小鼠哮喘样肺部炎症模型的可重复性
Clin Exp Immunol. 2004 May;136(2):224-31. doi: 10.1111/j.1365-2249.2004.02461.x.
2
Anti-tumor necrosis factor-alpha antibody treatment reduces pulmonary inflammation and methacholine hyper-responsiveness in a murine asthma model induced by house dust.抗肿瘤坏死因子-α抗体治疗可减轻由屋尘诱发的小鼠哮喘模型中的肺部炎症和乙酰甲胆碱高反应性。
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3
Eotaxin represents the principal eosinophil chemoattractant in a novel murine asthma model induced by house dust containing cockroach allergens.在一种由含蟑螂过敏原的屋尘诱发的新型小鼠哮喘模型中,嗜酸性粒细胞趋化因子是主要的嗜酸性粒细胞趋化剂。
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4
Reducing LPS content in cockroach allergens increases pulmonary cytokine production without increasing inflammation: a randomized laboratory study.降低蟑螂过敏原中的 LPS 含量可增加肺部细胞因子的产生而不增加炎症:一项随机实验室研究。
BMC Pulm Med. 2011 Feb 23;11:12. doi: 10.1186/1471-2466-11-12.
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CXC chemokines modulate IgE secretion and pulmonary inflammation in a model of allergic asthma.在过敏性哮喘模型中,CXC趋化因子可调节IgE分泌和肺部炎症。
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House dust bioactivities predict skin prick test reactivity for children with high risk of allergy.室内灰尘生物活性可预测过敏高风险儿童的皮肤点刺试验反应性。
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Endotoxin is not essential for the development of cockroach induced allergic airway inflammation.内毒素并非蟑螂诱导的过敏性气道炎症发展所必需。
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A dose-response relationship between exposure to cockroach allergens and induction of sensitization in an experimental asthma in Hartley guinea pigs.在哈特利豚鼠实验性哮喘中,蟑螂过敏原暴露与致敏诱导之间的剂量反应关系。
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Pulmonary endotoxin tolerance protects against cockroach allergen-induced asthma-like inflammation in a mouse model.肺部内毒素耐受可预防蟑螂过敏原诱导的哮喘样炎症反应。
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Early-life co-administration of cockroach allergen and endotoxin augments pulmonary and systemic responses.在生命早期同时给予蟑螂过敏原和内毒素会增强肺部和全身反应。
Clin Exp Allergy. 2009 Jul;39(7):1069-79. doi: 10.1111/j.1365-2222.2009.03254.x. Epub 2009 Apr 28.

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Inhibition of Epithelial CC-Family Chemokine Synthesis by the Synthetic Chalcone DMPF-1 via Disruption of NF-κB Nuclear Translocation and Suppression of Experimental Asthma in Mice.合成查耳酮DMPF-1通过破坏NF-κB核转位抑制上皮CC族趋化因子合成并抑制小鼠实验性哮喘
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Trif-dependent induction of Th17 immunity by lung dendritic cells.肺树突状细胞通过Trif依赖性诱导Th17免疫
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The Toll-like receptor 5 ligand flagellin promotes asthma by priming allergic responses to indoor allergens.Toll 样受体 5 配体鞭毛蛋白通过启动对室内过敏原的过敏反应促进哮喘。
Nat Med. 2012 Nov;18(11):1705-10. doi: 10.1038/nm.2920. Epub 2012 Oct 14.
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A2B adenosine receptor expression by myeloid cells is proinflammatory in murine allergic-airway inflammation.髓样细胞 A2B 腺苷受体的表达在小鼠变应性气道炎症中具有促炎作用。
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Cockroach allergens induce biphasic asthma-like pulmonary inflammation in outbred mice.蟑螂过敏原可在远交系小鼠中诱发双相性哮喘样肺部炎症。
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7
Endotoxin is not essential for the development of cockroach induced allergic airway inflammation.内毒素并非蟑螂诱导的过敏性气道炎症发展所必需。
Yonsei Med J. 2012 May;53(3):593-602. doi: 10.3349/ymj.2012.53.3.593.
8
Diesel exhaust particulates exacerbate asthma-like inflammation by increasing CXC chemokines.柴油机废气颗粒通过增加趋化因子 CXC 加剧类似哮喘的炎症。
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9
Reducing LPS content in cockroach allergens increases pulmonary cytokine production without increasing inflammation: a randomized laboratory study.降低蟑螂过敏原中的 LPS 含量可增加肺部细胞因子的产生而不增加炎症:一项随机实验室研究。
BMC Pulm Med. 2011 Feb 23;11:12. doi: 10.1186/1471-2466-11-12.
10
Inbred and outbred mice have equivalent variability in a cockroach allergen-induced model of asthma.在蟑螂过敏原诱导的哮喘模型中,近交系和远交系小鼠具有同等程度的变异性。
Comp Med. 2010 Dec;60(6):420-6.

本文引用的文献

1
Matrix metalloproteinase-9 deficiency results in enhanced allergen-induced airway inflammation.基质金属蛋白酶-9缺乏导致变应原诱导的气道炎症增强。
J Immunol. 2004 Feb 15;172(4):2586-94. doi: 10.4049/jimmunol.172.4.2586.
2
IgE-dependent enhancement of Th2 cell-mediated allergic inflammation in the airways.气道中IgE依赖的Th2细胞介导的过敏性炎症增强。
Clin Exp Immunol. 2004 Jan;135(1):12-8. doi: 10.1111/j.1365-2249.2004.02337.x.
3
Inhibition of Th1- and Th2-mediated airway inflammation by the sphingosine 1-phosphate receptor agonist FTY720.1-磷酸鞘氨醇受体激动剂FTY720对Th1和Th2介导的气道炎症的抑制作用
J Immunol. 2003 Dec 1;171(11):6206-14. doi: 10.4049/jimmunol.171.11.6206.
4
A recombinant fragment of human SP-D reduces allergic responses in mice sensitized to house dust mite allergens.人SP-D的重组片段可减轻对屋尘螨过敏原致敏小鼠的过敏反应。
Clin Exp Immunol. 2003 Nov;134(2):181-7. doi: 10.1046/j.1365-2249.2003.02281.x.
5
Targeted inactivation of the IL-4 receptor alpha chain I4R motif promotes allergic airway inflammation.IL-4受体α链I4R基序的靶向失活会促进过敏性气道炎症。
J Exp Med. 2003 Oct 20;198(8):1189-200. doi: 10.1084/jem.20030471. Epub 2003 Oct 13.
6
Antithetic regulation by beta-adrenergic receptors of Gq receptor signaling via phospholipase C underlies the airway beta-agonist paradox.β-肾上腺素能受体通过磷脂酶C对Gq受体信号传导的反向调节是气道β-激动剂悖论的基础。
J Clin Invest. 2003 Aug;112(4):619-26. doi: 10.1172/JCI18193.
7
Exposure to endotoxin and allergen in early life and its effect on allergen sensitization in mice.早期生活中接触内毒素和过敏原及其对小鼠过敏原致敏的影响。
J Allergy Clin Immunol. 2003 Aug;112(2):389-96. doi: 10.1067/mai.2003.1646.
8
Lipopolysaccharide-enhanced, toll-like receptor 4-dependent T helper cell type 2 responses to inhaled antigen.脂多糖增强的、依赖Toll样受体4的2型辅助性T细胞对吸入抗原的反应。
J Exp Med. 2002 Dec 16;196(12):1645-51. doi: 10.1084/jem.20021340.
9
Modification of acute and late-phase allergic responses to ovalbumin with lipopolysaccharide.脂多糖对卵清蛋白急性和迟发性过敏反应的调节作用
Int Arch Allergy Immunol. 2002 Oct;129(2):119-28. doi: 10.1159/000065881.
10
A reevaluation of the validity of unrestrained plethysmography in mice.对小鼠无约束体积描记法有效性的重新评估。
J Appl Physiol (1985). 2002 Oct;93(4):1198-207. doi: 10.1152/japplphysiol.00080.2002.

一种新型小鼠哮喘样肺部炎症模型的可重复性

Reproducibility of a novel model of murine asthma-like pulmonary inflammation.

作者信息

McKinley L, Kim J, Bolgos G L, Siddiqui J, Remick D G

机构信息

Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA.

出版信息

Clin Exp Immunol. 2004 May;136(2):224-31. doi: 10.1111/j.1365-2249.2004.02461.x.

DOI:10.1111/j.1365-2249.2004.02461.x
PMID:15086384
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1809026/
Abstract

Sensitization to cockroach allergens (CRA) has been implicated as a major cause of asthma, especially among inner-city populations. Endotoxin from Gram-negative bacteria has also been investigated for its role in attenuating or exacerbating the asthmatic response. We have created a novel model utilizing house dust extract (HDE) containing high levels of both CRA and endotoxin to induce pulmonary inflammation (PI) and airway hyperresponsiveness (AHR). A potential drawback of this model is that the HDE is in limited supply and preparation of new HDE will not contain the exact components of the HDE used to define our model system. The present study involved testing HDEs collected from various homes for their ability to cause PI and AHR. Dust collected from five homes was extracted in phosphate buffered saline overnight. The levels of CRA and endotoxin in the supernatants varied from 7.1 to 49.5 mg/ml of CRA and 1.7-6 micro g/ml of endotoxin in the HDEs. Following immunization and two pulmonary exposures to HDE all five HDEs induced AHR, PI and plasma IgE levels substantially higher than normal mice. This study shows that HDE containing high levels of cockroach allergens and endotoxin collected from different sources can induce an asthma-like response in our murine model.

摘要

对蟑螂过敏原(CRA)致敏被认为是哮喘的主要原因,尤其是在市中心人群中。革兰氏阴性菌的内毒素在减轻或加剧哮喘反应中的作用也已得到研究。我们创建了一种新型模型,利用含有高水平CRA和内毒素的屋尘提取物(HDE)来诱导肺部炎症(PI)和气道高反应性(AHR)。该模型的一个潜在缺点是HDE的供应有限,并且新制备的HDE不会包含用于定义我们模型系统的HDE的确切成分。本研究涉及测试从不同家庭收集的HDE引起PI和AHR的能力。从五个家庭收集的灰尘在磷酸盐缓冲盐水中过夜提取。上清液中CRA和内毒素的水平在HDE中从7.1至49.5 mg/ml的CRA和1.7 - 6μg/ml的内毒素不等。在免疫和两次肺部暴露于HDE后,所有五种HDE均诱导出AHR、PI和血浆IgE水平,显著高于正常小鼠。这项研究表明,从不同来源收集的含有高水平蟑螂过敏原和内毒素的HDE可以在我们的小鼠模型中诱导出类似哮喘的反应。