Galectin-10 mRNA is overexpressed in peripheral blood of aspirin-induced asthma

被引:41
作者
Devouassoux, G.
Pachot, A.
Laforest, L.
Diasparra, J.
Freymond, N.
Van Ganse, E.
Mougin, B.
Pacheco, Y.
机构
[1] Ctr Hosp Lyon Sud, Resp Dis Unit, HCL, F-69495 Pierre Benite, France
[2] UCB Lyon 1, EA 3091, Lyon, France
[3] Hop Edouard Herriot, Joint Unit Hospices Civils Lyon BioMerieux, Lyon, France
关键词
aspirin-induced asthma; aspirin-tolerant asthma; galectin-10; mRNA microarray; nasal polyposis;
D O I
10.1111/j.1398-9995.2007.01558.x
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
In sensitive patients, aspirin is associated with nasal and bronchial inflammation, eliciting local symptoms. Although the disease is clinically well characterized, its physiopathology is incompletely understood and noninvasive procedures, allowing an effective distinction between aspirin-induced asthma (AIA) and aspirin-tolerant asthma (ATA) are missing. The aims of the study were to compare AIA and ATA cohorts for clinical characteristics and to screen peripheral blood for differential mRNA expression. Patients experiencing symptoms following aspirin ingestion were considered as aspirin sensitive. Peripheral blood was collected to quantify mRNA expression, using microarray technology and quantitative RT-PCR. Data indicated that AIA and ATA share large number of similarities for clinical phenotype. Screening of mRNA expression using microarray showed an overexpression of galectin-10 mRNA in AIA (AIA/ATA ratio = 1.9, P < 0.05). Results were confirmed using qRT-PCR. A positive correlation was established between microarray and qRT-PCR results for galectin-10 mRNA expression (r = 0.92, P < 0.0001). Finally, qRT-PCR results were validated on a subset of asthmatics and controls, showing an increased expression of galectin-10 mRNA in AIA vs ATA (P < 0.001) and vs controls (P < 0.01). Our results demonstrate that AIA and ATA remain difficult to distinguish using clinical criteria. Employing two molecular biological methods, we demonstrate that galectin-10 mRNA is overexpressed in AIA, suggesting a novel candidate gene and a potentially innovative pathway for mucosal inflammation in aspirin intolerance.
引用
收藏
页码:125 / 131
页数:7
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