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Single nucleotide polymorphisms (SNPs) close to the gain-of-function substitution, Asn(107)Ile (rs324981, A>T), in Neuropeptide S Receptor 1 ( NPSR1 ) have been associated with asthma. Furthermore, a functional SNP (rs4751440, G>C) in Neuropeptide S  (NPS)  encodes a Val(6)Leu substitution on the mature peptide that results in reduced bioactivity. We sought to examine the effects of different combinations of these  NPS  and  NPSR1  variants on downstream signaling and genetic risk of asthma. In transfected cells, the magnitude of NPSR1-induced activation of cAMP/PKA signal transduction pathways and downstream gene expression was dependent on the combination of the NPS and NPSR1 variants with NPS-Val(6)/NPSR1-Ile(107) resulting in strongest and NPS-Leu(6)/NPSR1-Asn(107) in weakest effects, respectively. One or two copies of the NPS-Leu(6) (rs4751440) were associated with physician-diagnosed childhood asthma (OR: 0.67, 95%CI 0.49–0.92, p = 0.01) and together with two other linked  NPS  variants (rs1931704 and rs10830123) formed a protective haplotype (p = 0.008) in the Swedish birth cohort BAMSE (2033 children).  NPS  rs10830123 showed epistasis with  NPSR1  rs324981 encoding Asn(107)Ile (p = 0.009) in BAMSE and with the linked  NPSR1  rs17199659 (p = 0.005) in the German MAGIC/ISAAC II cohort (1454 children). In conclusion,  NPS  variants modify asthma risk and should be considered in genetic association studies of  NPSR1  with asthma and other complex diseases.

Neuropeptide S (NPS) variants modify the signaling and risk effects of NPS Receptor 1 (NPSR1) variants in asthma