Abousaidi Hamid, Vazirinejad Reza, Arababadi Mohammad Kazemi, Rafatpanah Houshang, Pourfathollah Ali Akbar, Derakhshan Reza, Daneshmandi Saeed, Hassanshahi Gholamhossein
Department of Infectious Disease, Rafsanjan Ali Ebne Abitaleb Hospital, Rafsanjan, Iran.
South Med J. 2011 Jun;104(6):422-5. doi: 10.1097/SMJ.0b013e3182186ff0.
Chemokines and their receptors are clinically important mediators, as the chemokine receptors are expressed on almost all immune cells. They play pivotal roles in pathogenesis of almost all clinical situations including asthma. Correspondingly, MIP-1α (CCL3), MIP-1β (CCL4), and RANTES (CCL5) are among the important chemokines involved in the pathogenesis of asthma. These chemokines bind to the CCR5 (their related receptor) on the cell surfaces. Attachment of related chemokine ligands to CCR5 plays an important role in the pathogenesis of asthma; hence, this study aimed to analyze δ32 mutations in CCR5 in asthmatic patients.
This experimental study was undertaken on 162 asthmatic patients and 200 healthy controls during February to June 2008 at Rafsanjan University of Medical Sciences. The Gap-PCR method was applied to analyze the δ32 mutation in the CCR5 gene, and demographic data (eg, age, sex, occupation, socio-economic status) were collected using a questionnaire.
The findings of this study indicated that none of the asthmatic patients exhibited δ32 mutation in CCR5 chemokine receptor while only 3 (1.5%) of controls had the heterozygotic form of this mutation.
Several research groups analyzed δ32 mutations in CCR5 in different diseases, including asthma. Some investigations reported a significant relation between asthma and δ32 mutations in CCR5, but there are also many reports which failed to find a relation between asthma and this mutation. Based on the results of this study and others, it seems that the δ32 mutation does not affect the pathogenesis of asthma.
趋化因子及其受体是临床上重要的介质，因为趋化因子受体几乎在所有免疫细胞上都有表达。它们在包括哮喘在内的几乎所有临床病症的发病机制中都起着关键作用。相应地，巨噬细胞炎性蛋白-1α（CCL3）、巨噬细胞炎性蛋白-1β（CCL4）和调节激活正常T细胞表达和分泌因子（CCL5）是参与哮喘发病机制的重要趋化因子。这些趋化因子与细胞表面的CCR5（它们的相关受体）结合。相关趋化因子配体与CCR5的结合在哮喘发病机制中起重要作用；因此，本研究旨在分析哮喘患者中CCR5的δ32突变。
2008年2月至6月，在拉夫桑詹医科大学对162例哮喘患者和200例健康对照进行了这项实验研究。采用缺口聚合酶链反应（Gap-PCR）方法分析CCR5基因中的δ32突变，并通过问卷收集人口统计学数据（如年龄、性别、职业、社会经济地位）。
本研究结果表明，哮喘患者中无一例在CCR5趋化因子受体中表现出δ32突变，而对照组中只有3例（1.5%）具有这种突变的杂合形式。
几个研究小组分析了不同疾病（包括哮喘）中CCR5的δ32突变。一些研究报告了哮喘与CCR5的δ32突变之间存在显著关系，但也有许多报告未能发现哮喘与该突变之间的关系。基于本研究及其他研究结果，似乎δ32突变不影响哮喘的发病机制。
