The diagnostic value of serum levels of brain-derived neurotropic factor (BDNF) and bdnf val66met polymorphism in patients with irritabl bowel syndrome (İBS)

Introduction: Irritable bowel syndrome (IBS) is a functional bowel disease characterized by abdominal discomfort, changes in the form and frequency of defecation. Although its etiology is not fully known, it is thought to be caused by many factors such as psychological factors, nutritional habits and changes in intestinal flora. The brain-bowel axis can be defined as a bidirectional connecting system that uses autonomic neural, neuroimmune, and neuroendocrine pathways between the gastrointestinal tract (enteric nervous system) and the brain (central nervous system). Therefore, when bowel function is impaired, this may also be caused by modulator inputs from the central nervous system in the brain-bowel axis. Neurotrophins are a quite important family of growth factors for the regulation of neuronal care, differentiation, and survival. Among these, dysregulation of brain-derived neurotrophic factor (BDNF) is known to increase susceptibility to neurodegenerative diseases. BDNF is widely distributed in different regions of the intestinal tractus such as enteric nervous system neurons, intestinal mucosa epithelium, interstitial space. There are many studies investigating the physiological effects of BNDF on intestinal motility. An aminoacid exchange (rs6265) from valine (Val) to methionine (Met) at position 66 within the pro-region of BDNF causes a functional single nucleotide polymorphism (SNP). Within the scope of this project, the relationship between IBS and BNDF polymorphism and serum BDNF levels were examined. Patients and Methods: 60 patients and 40 healthy individuals who were admitted to the Düzce University Research and Practice Hospital Internal Diseases and Gatroenterology outpatient clinics between January 2019 and September 2019 and diagnosed with IBS according to ROME 4 criteria were determined on a voluntary basis. In serum samples of patients, BDNF levels are in the 96-well ELISA plates coated with human BDNF monoclonal antibodies to the manufacturer's study protocol with the commercially purchased "Human Free BDNF Quantikine ELISA" test kit (R&D Systems, Inc., Minneapolis, MN, USA). It was appropriately analyzed at the quantitative level. In addition, BDNF genotyping was performed by DNA extraction from whole blood samples and subsequently by PCR-RLFP analysis. BDNF ELISA test and BDNF genotyping were studied in Karabuk University Faculty of Medicine Department of Medical Biology. Results: Mean serum BDNF levels were found as 781,888 pg / mL (128,48-1501,6) in the patient group and 988,715 pg / mL (66,1-1948,8) in the control group. Mean BDNF levels were significantly lower in the patient group (p=0.019) when compared to healthy controls. When the IBS subgroup analysis was performed, a significant decrease was found in the mean BDNF level in the IBS-I subgroup. There were no significant differences between the mean levels of BDNF for psychiatric history of disease, psychiayric drug use or smoking (p>0.05). Val and Met allele frequencies were evaluated between the patient and control groups. There was no significant difference between the genotypes and allele frequencies of the patient and control groups (p = 0.499). Met allele frequency was found to be 17% in the patient group and 12,5% in the control group. There was no significant association between BDNF levels and genotypes of the patients (p>0,05). Conclusion: As a result of our study, we found that serum BDNF level was lower in patients with IBS compared to the control group. However, there was no significant difference in genotype in the patient and control groups. We also found that there was no significant association between BDNF gene polymorphism and serum BDNF levels. This may be due to the fact that the BDNF gene has dynamic functional regulation and has various expression patterns in different tissues and pathologies. Therefore, the study should be conducted in a wider group of patients and therefore increasing the frequency of Met alleles may provide statistically more accurate results. We hope that our study will shed light on the wider and controlled work to be done on this issue.