COX2 and p53 risk-alleles coexist in COPD.

Abstract Background Cigarette smoke stimulates airway epithelial cells to release pro-inflammatory cytokines which influence various inflammation-related genes, including COX2 , whereas p53 expression is known to alter in such a condition. Since both the genes share several common physiological functions including inflammation and oxidative stress, we investigated within gene and gene–gene interactions towards susceptibility to the disease. Method In a prospective gene-association study we conducted PCR-RFLP for genotyping the COX2 −765G/C and 8473T/C and p53 72Pro/Arg polymorphisms in 229 COPD patients and 147 healthy controls. Results The −765GC+CC genotypes of COX2 and Pro/Pro+Pro/Arg genotypes of p53 were prevalent in patients with significant odds ratio, 2.05 and 2.30, respectively ( p  = 0.001; p  = 0.009, respectively), as a consequence, the −765C and 72Pro alleles were prevalent ( p  ≤ 0.001). Individually, the 8473T/C polymorphism did not associate with the disease ( p  = NS), however, it did in the haplotype −765C:8473C, which was significantly higher in patients ( p p  = 0.0004). The pairwise gene–gene interactions validated prevalence of risk-alleles associated pairing of genotypes such as the Pro/Pro+ Pro/Arg with −765GC+−765CC in patients ( p  = 0.01). Conclusion The prevalence of COX2 and p53 risk-alleles contributes towards susceptibility to the disease.