Identification of hub genes and key pathways between celiac and Crohn's diseases via bioinformatics tools

Abstract

Background: Chronic inflammatory diseases are the long-term response of the organism to any stimulus. Crohn's (CD) and Celiac (CeD) diseases are among chronic inflammatory diseases, and both cause chronic inflammation in the intestines. Both diseases are caused by polygenic, environmental, and lifestyle risk factors. Inflammation can perpetuate disease and cause it to become chronic. For this reason, CD and CeD that choose the intestine as the target organ may trigger each other. Although the relationship between these diseases is widely mentioned in the literature, scanty knowledge and research have been done on the immune mechanisms of these inflammatory diseases. Aim: This study aimed to determine hub genes, transcription factors-miRNAs, and protein-chemical interaction networks shared between CD and CeD. Methods: The NCBI-GEO datasets were downloaded and analyzed in GEO2R to identify differentially expressed genes (DEGs). STRING tool for Protein -Protein Interaction (PPI) and NetworkAnalyst tool were used for Gene Set Enrichment Analysis (GSEA), Transcription factor (TF) -miRNA Coregulatory Networks, and Protein-Chemical Interactions. Results and Discussion: GSE11501 and GSE3365 datasets were utilized to recognize 54 DEGs in CD, and CeD. 13 of these commonly expressed genes were defined as hub genes. GSEA has indicated that these genes are associated with immune system processes, cellular defense response, proteolysis, and apoptosis. KAT6A and SPI1 are transcription factors that direct the continuity of intestinal epithelial cells. Antirheumatic agents and Methotrexate are likely to be used to treat these diseases. Conclusions: In conclusion, we think that delayed-type hypersensitivity resulting from epitope propagation is a common immune mechanism of CD and CeD. Given the increasing prevalence of both CD and CeD in the population, it is clear that more studies are needed to understand the shared pathogenesis and overlapping immune mechanisms of these diseases.