Abstract
Autoimmune hepatitis (AIH) is a special type of chronic liver disease caused by immune dysfunction in the body. This study aims to explore the molecular regulatory mechanisms of inflammation and fibrosis in AIH. Bioinformatics was used to screen differentially expressed genes in autoimmune hepatitis and reveal core gene functions. The autoimmune hepatitis dataset GSE9892 generated by GPL1261 was obtained by gene expression omnibus. Functional enrichment analysis, weighted gene co-expression network analysis, construction and analysis of protein-protein interaction network and comparative toxicogenomics database analysis were performed. A heat map of gene expression was drawn. A total of 3080 differentially expressed genes were identified. Gene ontology analysis revealed that these genes were mainly involved in organic acid catabolism processes, condensed centromeric chromosomal regions and oxidoreductase activity. Kyoto encyclopedia of genes and genomes analysis showed that they were mainly associated with the NOD-like receptor signaling pathway, the Toll-like receptor signaling pathway, the TNF signaling pathway, the Jak-STAT signaling pathway and the T cell receptor signaling pathway. Metascape enrichment analysis revealed that gene ontology enrichment highlighted processes including innate immune response, regulate immune response, inflammatory response, leukocyte activation, regulate cell activation, regulate cytokines, regulate immune system processes, regulate immune effector processes, immune activation, leukocyte migration, degranulation, myeloid activation, and viral response. Five core genes (Cxcl10, Ptprc, Cd86, Tnf, and small nucleolar RNA host gene 7 [SNHG7]). Heatmap of core gene expression showed that SNHG7 was down-regulated in the autoimmune hepatitis samples and up-regulated in the normal samples. Comparative toxicogenomics database analysis showed that SNHG7 is associated with chronic progressive liver inflammation, fever, fatigue, abdominal distension and tenderness of the liver. SNHG7 was down-regulated in the AIH, and it might be unique biomarker of AIH.