Abstract
Background Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) refers to a common disorder with unclear etiology and unsatisfactory treatment, which reduces the male's quality of life. Objective To examine the effects of genetic polymorphisms of IFNG, IFNGR1, and androgen receptor (AR) on CP/CPPS. Methods The single nucleotide polymorphisms (SNPs) of IFNG, IFNGR1, and AR were genotyped with the improved multiplex ligation detection reaction. The GTEx, RegulomeDB, HaploReg, and 3DSNP databases were adopted to predict the regulatory functions of the genotyped SNPs. The correlation between SNPs and CP/CPPS was analyzed with the χ2 test, logistic regression, and two genetic models (codominant and log-additive models). The nomogram was built to predict the risk of CP/CPPS occurrence. Results On the whole, 130 CP/CPPS patients and 125 healthy controls were recruited in the study, and 18 SNPs of IFNG, IFNGR1, and AR were genotyped. The results of functional annotation indicated that the 18 genotyped SNPs might have regulatory effects in the whole blood. The rs144488434 was correlated with the elevated CP/CPPS risk (odds ratio (OR): 2.40, 95% confidence interval (CI): 1.12-5.13, χ2 = 5.37, and P = 0.021) by the χ2 test. In the built genetic models, rs10457655 was correlated with the elevated National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) scores (codominant model: GA/GG: crude mean difference (MD) = 0.98, 95% CI: -1.71-3.67 and AA/GG: crude MD = 9.10, 95% CI: 0.58-17.62, P = 0.10). In subgroup analysis, rs2069718 was correlated with the elevated CP/CPPS risk (log-additive model: crude OR = 2.18, 95% CI: 1.03-4.64, and P = 0.034) in patients ≥ 35 years. The nomogram integrating age, rs2069718, rs10457655, and rs144488434 showed good performance to predict the risk of CP/CPPS. Conclusions Genetic polymorphisms of IFNG, IFNGR1, and AR might act as the genetic factors for CP/CPPS susceptibility, which deserved further explorations.
Highlights
According to the National Institutes of Health (NIH) classification, chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is defined as category III prostatitis, affecting approximately 8.4% to 25% of males worldwide [1, 2]
By analyzing genetic polymorphisms of tumor necrosis factor- (TNF-) α and interleukin(IL-) 10, Shoskes et al reported that CPPS patients had a higher proportion of low IL-10 production genotype, and the symptoms of patients with high IL-10 and low TNF-α phenotypes were not mitigated by anti-inflammatory phytotherapy [4]
The information of the 18 single nucleotide polymorphisms (SNPs), minor allele frequency (MAF), and Hardy-Weinberg equilibrium (HWE) test are listed in Supplemental Table 1
Summary
According to the National Institutes of Health (NIH) classification, chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is defined as category III prostatitis, affecting approximately 8.4% to 25% of males worldwide [1, 2]. Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) refers to a common disorder with unclear etiology and unsatisfactory treatment, which reduces the male’s quality of life. To examine the effects of genetic polymorphisms of IFNG, IFNGR1, and androgen receptor (AR) on CP/CPPS. The GTEx, RegulomeDB, HaploReg, and 3DSNP databases were adopted to predict the regulatory functions of the genotyped SNPs. The correlation between SNPs and CP/CPPS was analyzed with the χ2 test, logistic regression, and two genetic models (codominant and logadditive models). 130 CP/CPPS patients and 125 healthy controls were recruited in the study, and 18 SNPs of IFNG, IFNGR1, and AR were genotyped. In the built genetic models, rs10457655 was correlated with the elevated National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) scores (codominant model: GA/GG: crude mean difference ðMDÞ = 0:98, 95% CI: -1.71-3.67 and AA/GG: crude MD = 9:10, 95% CI: 0.58-17.62, P = 0:10). Genetic polymorphisms of IFNG, IFNGR1, and AR might act as the genetic factors for CP/CPPS susceptibility, which deserved further explorations
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