BACKGROUND: The secretory protein, uteroglobin-related protein 1 (UGRP1), is mainly expressed in the lung and trachea and has recently been implicated in asthma. The -112 G to A transition in the promoter was reported to be associated with asthma in the Japanese population. However, this has not been replicated in other studies. The aim of this study was to find the association of UGRP1 gene polymorphisms with atopic asthma in the Indian population using a case-control (NP=165, NC=160) and a family-based (60 trios) design. METHODS: Polymorphisms in the promoter region and the first exon and first intron of the UGRP1 gene were determined by direct sequencing. RESULTS: The previously identified G-112A and C222A polymorphisms were found to be in complete linkage disequilibrium (LD) (D'=1) in our population. However, no new polymorphism has been identified in this region. When G-112A polymorphism was analyzed in the cases and controls, no significant difference was observed either at the allele (p=0.68) or at the genotype (p=0.83) levels. Moreover, in our family-based study, we observed no significant deviation of allelic transmission from random proportions (p=0.41). Similarly, when we analyzed our genotypic results for serum total IgE levels, no significant association was observed, in both case-control as well as family-based designs. CONCLUSIONS: Our results suggest that the G-112A and C222A polymorphisms do not play a significant role in the genetic predisposition of UGRP1 gene in atopic asthma in the Indian population.
BACKGROUND: The secretory protein, uteroglobin-related protein 1 (UGRP1), is mainly expressed in the lung and trachea and has recently been implicated in asthma. The -112 G to A transition in the promoter was reported to be associated with asthma in the Japanese population. However, this has not been replicated in other studies. The aim of this study was to find the association of UGRP1 gene polymorphisms with atopic asthma in the Indian population using a case-control (NP=165, NC=160) and a family-based (60 trios) design. METHODS: Polymorphisms in the promoter region and the first exon and first intron of the UGRP1 gene were determined by direct sequencing. RESULTS: The previously identified G-112A and C222A polymorphisms were found to be in complete linkage disequilibrium (LD) (D'=1) in our population. However, no new polymorphism has been identified in this region. When G-112A polymorphism was analyzed in the cases and controls, no significant difference was observed either at the allele (p=0.68) or at the genotype (p=0.83) levels. Moreover, in our family-based study, we observed no significant deviation of allelic transmission from random proportions (p=0.41). Similarly, when we analyzed our genotypic results for serum total IgE levels, no significant association was observed, in both case-control as well as family-based designs. CONCLUSIONS: Our results suggest that the G-112A and C222A polymorphisms do not play a significant role in the genetic predisposition of UGRP1 gene in atopic asthma in the Indian population.