Eicosanoid mediator expression in mononuclear and polymorphonuclear cells in normal subjects and patients with atopic asthma and cystic fibrosis.
Eicosanoid mediator expression in mononuclear and polymorphonuclear cells in normal subjects and patients with atopic asthma and cystic fibrosis.
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正常受试者和特应性哮喘和囊性纤维化患者的单核和多形核细胞中类二十烷酸介质的表达。
作者：
L. Kuitert;R. Newton;N. Barnes;I. Adcock;P. Barnes
背景技术背景：类二十烷酸如白三烯、洋地黄素、脂氧素和15-氢过氧二十碳四烯酸（15-HETE）引起支气管收缩、微血管通透性增加、粘液分泌和多形物趋化性。这些促炎作用在诸如哮喘和囊性纤维化的疾病中是重要的，其中介质的水平在稳定和急性状态下都增加。进行了一项研究以检测正常受试者和患有稳定的特应性哮喘和稳定的囊性纤维化的患者中类花生酸途径的酶（5-脂氧合酶（5-LO）、5-脂氧合酶激活蛋白（FLAP）、环加氧酶1和2（考克斯-1、考克斯-2）和15-脂氧合酶（15-LO））的mRNA表达。方法：采用逆转录聚合酶链反应（RT-PCR）检测3组患者外周血多形核细胞和单个核细胞中5-LO、FLAP、考克斯-1、考克斯-2和15-LO的总RNA表达。结果：5-LO和FLAP的mRNA表达在正常人、哮喘和囊性纤维化患者中相似。考克斯-1在哮喘患者的两种细胞类型中均增加。考克斯-2和15-LO在过敏性哮喘患者的多形核细胞中增加，但在单个核细胞中不增加。考克斯-2和15-LO在囊性纤维化患者的两种细胞类型中均未检测到，而考克斯-1在多态性中的水平与哮喘患者相似。结论：哮喘和囊性纤维化中白三烯产生的增加不能用5-LO和FLAP转录的增加来解释。特应性哮喘患者15-LO和考克斯-2的转录水平升高。考克斯-1的转录在特应性哮喘和囊性纤维化中均增加。
BACKGROUND: Eicosanoids such as leukotrienes, prostaglandins, lipoxins, and 15-hydroperoxyeicosatetraenoic acid (15-HETE) cause bronchoconstriction, increased microvascular permeability, mucus secretion, and polymorph chemotaxis. These pro-inflammatory effects are important in diseases such as asthma and cystic fibrosis where the levels of mediators are increased both in the stable and acute state. A study was conducted to examine the expression of the mRNA for the enzymes of the eicosanoid pathways (5-lipoxygenase (5-LO), 5-lipoxygenase activating protein (FLAP), cyclo-oxygenases 1 and 2 (COX-1, COX-2), and 15-lipoxygenase (15-LO)) in normal subjects and in patients with stable atopic asthma and stable cystic fibrosis. METHODS: Reverse transcription polymerase chain reaction (RT-PCR) was used to examine the expression of total RNA for 5-LO, FLAP, COX-1, COX-2, and 15-LO in peripheral blood polymorphonuclear cells and mononuclear cells from the three subjects groups. RESULTS: The expression of mRNA for 5-LO and FLAP was similar in normal subjects and in patients with asthma and cystic fibrosis. COX-1 was increased in both cell types in asthmatic patients. COX-2 and 15-LO were increased in polymorphs of patients with atopic asthma but not in mononuclear cells. COX-2 and 15-LO were undetectable in either cell type in patients with cystic fibrosis whereas COX-1 levels in polymorphs were similar to those in patients with asthma. CONCLUSIONS: The increased leukotriene production in asthma and cystic fibrosis is not explained by an increase in transcription of 5-LO and FLAP. Transcription of 15-LO and COX-2 is increased in atopic asthma. Transcription of COX-1 is increased in both atopic asthma and cystic fibrosis.
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DOI：
10.1152/jappl.1992.73.2.781
发表时间：
1992
期刊：
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子：
--
作者：
Pueringer,RJ;Bahns,CC;Hunninghake,GW
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Hunninghake,GW
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DOI：
--
发表时间：
1994
期刊：
Advances in prostaglandin, thromboxane, and leukotriene research
影响因子：
--
作者：
Sigal,E;Conrad,DJ
通讯作者：
Conrad,DJ
影响因子：
15.9
作者：
HEMPEL, SL;MONICK, MM;HUNNINGHAKE, GW
通讯作者：
HUNNINGHAKE, GW
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DOI：
--
发表时间：
1992
期刊：
Kidney international. Supplement
影响因子：
--
作者：
Badr,KF
通讯作者：
Badr,KF
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DOI：
--
发表时间：
1987
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Bigby,TD;Holtzman,MJ
通讯作者：
Holtzman,MJ