NPSR1 gene gene link to asthma and atopy confirmed
MedWire News: Study results confirm a link between variants of the neuropeptide S receptor 1 gene (NPSR1) and the development of asthma and atopy, particularly early-onset asthma.
M Kogevinas (Centre for Research in Environmental Epidemiology, Barcelona, Spain) and team explain that previous studies have identified five candidate genes encoding ADAM metallopeptidase domain 33 (ADAM33), PHD finger protein 11 (PHF11), neuropeptide S receptor 1 (NPSR1), dipeptidyl-peptidase 10 (DPP10), and serine protease inhibitor kazal type 5 (SPINK5) that may be associated with the development of asthma, atopy and bronchial hyper-responsiveness (BHR).
To investigate further, the researchers genotyped 4331 individuals, aged 20–44 years from 13 countries who participated in the European Community Respiratory Health Survey (1990–2000), for single nucleotide polymorphisms (SNPs) in the candidate genes.
As reported in the journal Thorax, 51 SNPs were studied in 2166 participants with asthma, atopy, and/or BHR and 1213 controls without these conditions.
The researchers found that only the NPSR1 gene showed significant associations with asthma and atopy, with three SNPs (rs184448, rs324957, rs324981) associated with asthma and one with atopy (rs324396).
The associations between NPSR1 and asthma were particularly strong for disease onset before the age of 15 years, the researchers note.
They also found nonsignificant age-specific associations for two SNPs in DPP10 and asthma development.
For BHR, one significant association was found regarding an SNP (rs2787095) in ADAM33, but this did not pass further analysis.
Kogevinas and team conclude: “This study gives independent support to NPSR1 as a risk factor for asthma, atopy, and atopic asthma.
“In addition, this analysis adds evidence to the importance of considering age-specific effects in evaluating the genetic risk factors in asthma, suggesting a role for NPSR1 in early-onset asthma driven by the strong effect of this gene on atopic asthma.”
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By Mark Cowen