Evaluating the association between genetic polymorphisms of calprotectin and inflammatory bowel diseases

According to the epidemiological studies, manifestations of chronic inflammatory bowel diseases (IBD) are different in various parts of the world. Calprotectin, a complex of two S100A8 and S100A9 proteins, is one of the major mediators of inflammation in patients with inflammatory bowel disease. This study was aimed to investigate the genetic single nucleotide polymorphism (SNP) of calprotectin in ulcerative colitis and crohn’s disease patients and its association with the disease behaviors. One hundred and sixty six patients with inflammatory bowel disease (ulcerative colitis or crohn’s disease) were included in the study. A volume of 2 mL venous blood samples were collected and DNA samples purified. The target regions of calprotectin genes, including S100A8 (rs3806232) and S100A9 (rs3014866) were amplified by polymerase chain reaction (PCR) method. The relationship between polymorphism of calprotectin and age, sex, extension, flare, disease severity (according to the administered drugs), extra intestinal manifestations (arthritis, primary sclerosing cholangitis, eye and skin involvement), dysplasia, colon cancer and were evaluated. Analysis of data showed that CT genotype of S100A9 and TT genotype of S100A8 were the most common genotypes (P < 0.05). Majority of patients with arthritis showed CC genotype of S100A9 (P < 0.05). No significant differences were observed between the age, sex, incidence of extra intestinal manifestations and calprotectin genotype. TT genotype of S100A8 gene had a significant relationship with patients received the second-line drugs including corticosteroids and azathioprine (P < 0.05). Although, a significant association was not observed between patients with 1 to 2 flare in a year and calprotectin genotypes in our study, but 3 times annual flares were significantly more common in CC genotype of S100A9 gene than the other genotypes (P < 0.05). Our study results suggest genetic polymorphisms of calprotectin could affect IBD features including disease severity (based on the drugs needed to control the disease), extra intestinal manifestations (arthritis) and disease flare. This is, to our knowledge, the first investigation on the genetic polymorphisms of calprotectin in the inflammatory bowel diseases. Further investigation is really needed to confirm the role of calprotectin genotypes in the development of inflammatory bowel disease and their relationships with disease activity and features.