Effects of STIP1 and GLCCI1 polymorphisms on the risk of childhood asthma and inhaled corticosteroid response in Chinese asthmatic children

Abstract

Background: Asthma is a common chronic lung disease in children. We aimed to determine the associations between stress-induced phosphoprotein 1 (STIP1) and glucocorticoid-induced transcript 1 (GLCCI1) polymorphisms and susceptibility of childhood asthma and inhaled corticosteroid (ICS) response in children. Methods: A total of 263 Chinese Han asthmatic children were recruited from the Xiangya Hospital, Central South University. Pulmonary function tests were performed before the treatment and 3 months after the treatment. 150 non-asthmatic children were recruited. Each participant's DNA was extracted from the peripheral blood and Method of MassARRAY was used to genotype the single-nucleotide polymorphisms (SNPs). Results: STIP1 rs2236647 wild-type homozygote (CC) was associated with increased asthma risk of children (OR=1.858，95% CI：1.205-2.864), but not associated with the onset age of asthma and ICS response. GLCCI1 rs37969, rs37972 and rs37973 polymorphisms were not associated with the risk of childhood asthma. However, rs37969 mutant genotypes (TT/GT) were significantly associated with increased risk of early onset asthma (OR=2.254, 95% CI: 1.068-4.757) and less improvement in PD20 (p = 0.028). We also found significant associations between rs37969, rs37972 and rs37973 mutant genotypes and less improvement in maximal midexpiratory flow (MMEF) after ICS treatment for 3 months (p=0.036, p=0.010 and p=0.003, respectively). Conclusions: STIP1 rs2236647 was associated with asthma risk of children. GLCCI1 rs37969 mutant genotypes were associated with increased asthma risk of early onset and less improvement in airway hyper-responsiveness. GLCCI1 rs37969, rs37972 and rs37973 polymorphisms might be associated with pulmonary function in childhood asthma patients after ICS treatment.

GLCCI1 reduces collagen deposition and airway hyper‐responsiveness in a mouse asthma model through binding with WD repeat domain 45B

“…asthma, autophagy, glucocorticoid-induced transcript 1 gene, WD repeat domain 45B hyper-responsiveness. 7 In our previous study, we found that expression of GLCCI1 is associated with the changes of forced expiratory volume in 1 second in asthmatic patients accepted with fluticasone propionate treatment. 8 Moreover, in our previous study, we also demonstrated that knockout GLCCI1 in asthmatic mice could attenuate the therapeutic outcome of hydroprednisone.…”