Abstract

Background: 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-1 alpha (CCL3), MIP-1 beta (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 delta 32 mutations in CCR5 in asthmatic patients. Material and Methods: 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 delta 32 mutation in the CCR5 gene, and demographic data (eg, age, sex, occupation, socioeconomic status) were collected using a questionnaire. Results: The findings of this study indicated that none of the asthmatic patients exhibited delta 32 mutation in CCR5 chemokine receptor while only 3 (1.5) of controls had the heterozygotic form of this mutation. Discussion: Several research groups analyzed delta 32 mutations in CCR5 in different diseases, including asthma. Some investigations reported a significant relation between asthma and delta 32 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 delta 32 mutation does not affect the pathogenesis of asthma.