Nikolaos-Panagiotis Andreou1, Evangelia Legaki1, Nikolas Dovrolis2, Nikola Boyanov3, Konstantinos Georgiou4, Kalliopi Gkouskou5, Maria Gazouli6. 1. Laboratory of Biology, Medical School, National and Kapodistrian University of Athens, Michalakopoulou 176, 11527 Athens, Greece. 2. Laboratory of Medical Biology, Department of Medicine, Democritus University of Thrace, Alexandroupolis, Greece. 3. Medical Simulation Training Center at Research Institute of Medical University of Plovdiv, Plovdiv, Bulgaria. 4. First Department of Propaedeutic Surgery, Hippokration General Hospital of Athens, Athens Medical School, National and Kapodistrian University of Athens, Athens, Greece. 5. Laboratory of Biology, Medical School, National and Kapodistrian University of Athens, Michalakopoulou 176, 11527 Athens, Greece; Embiodiagnostics, Biology Research Company, Heraklion, Crete, Greece. 6. Laboratory of Biology, Medical School, National and Kapodistrian University of Athens, Michalakopoulou 176, 11527 Athens, Greece. Electronic address: mgazouli@med.uoa.gr.
Abstract
BACKGROUND: Several studies correlated elevated B-cell activating factor (BAFF) levels and its polymorphisms (SNPs) in patients with autoimmunity. Limited data existed regarding the role of BAFF in Crohn's Disease (CD) susceptibility and/or treatment response to infliximab. AIM: This study aims to evaluate BAFF expression in CD patients, investigate if its expression can predict response to infliximab treatment, and examine the association of BAFF SNPs with CD susceptibility. METHODS: One hundred twelve CD patients and 164 healthy controls were recruited. Serum BAFF levels were determined using an enzyme-linked immunosorbent assay. Participants were genotyped for rs9514828, rs1041569 and rs2893321 SNPs. RESULTS: Serum BAFF concentration was elevated in CD patients (472.86 ± 223.60 pg/ml) compared with controls (128.16 ± 70.10 pg/ml) before treatment. Responders to IFX treatment had increased serum BAFF levels at baseline (610.03 ± 167.55 pg/ml) compared to non-responders (267.09 ± 107 pg/ml). In responders, BAFF concentration reduced after IFX administration, while increased in non-responders. The rs1041569, TA and AA genotypes frequencies, and the minor allele A were increased significantly in CD patients, indicating an association of the SNP with CD susceptibility. CONCLUSIONS: Our study suggests that BAFF could be a potential biomarker of CD, while SNP rs1041569 was associated with CD susceptibility.
BACKGROUND: Several studies correlated elevated B-cell activating factor (BAFF) levels and its polymorphisms (SNPs) in patients with autoimmunity. Limited data existed regarding the role of BAFF in Crohn's Disease (CD) susceptibility and/or treatment response to infliximab. AIM: This study aims to evaluate BAFF expression in CD patients, investigate if its expression can predict response to infliximab treatment, and examine the association of BAFF SNPs with CD susceptibility. METHODS: One hundred twelve CD patients and 164 healthy controls were recruited. Serum BAFF levels were determined using an enzyme-linked immunosorbent assay. Participants were genotyped for rs9514828, rs1041569 and rs2893321 SNPs. RESULTS: Serum BAFF concentration was elevated in CD patients (472.86 ± 223.60 pg/ml) compared with controls (128.16 ± 70.10 pg/ml) before treatment. Responders to IFX treatment had increased serum BAFF levels at baseline (610.03 ± 167.55 pg/ml) compared to non-responders (267.09 ± 107 pg/ml). In responders, BAFF concentration reduced after IFX administration, while increased in non-responders. The rs1041569, TA and AA genotypes frequencies, and the minor allele A were increased significantly in CD patients, indicating an association of the SNP with CD susceptibility. CONCLUSIONS: Our study suggests that BAFF could be a potential biomarker of CD, while SNP rs1041569 was associated with CD susceptibility.