Abstract
Abstract Background Allergic contact dermatitis (ACD) is a typical T cell-mediated inflammatory skin disorder driven by a cascade of dysregulated inflammatory signaling pathways. Aim The present study aimed to clarify the molecular pathways by which miR-155-5p regulates the inflammatory responses associated with ACD. Method Patients with clinically suspected ACD after urostomy were recruited as the clinically suspected ACD group, and patients with uncomplicated urostomy were included as the control group, with 110 cases in each group. miR-155-5p and SOCS1 levels were quantified using real-time quantitative polymerase chain reaction (RT-qPCR). Cell biological function was determined via transfection and cell counting kit-8 (CCK-8) assays, and the levels of inflammatory cytokines and T-cell chemokines were measured using enzyme-linked immunosorbent assay (ELISA). Western blot analysis was performed to detect the expression levels of relevant proteins. The connection between miR-155-5p and SOCS1 was confirmed by bioinformatics prediction and luciferase activity assays. Result miR-155-5p expression was upregulated in the clinically suspected ACD group and in HaCaT cells stimulated with TNF-α and IFN-γ (TI). Notably, downregulation of miR-155-5p promoted apoptosis and attenuated the production of inflammatory cytokines and T-cell chemokines. In contrast, silencing of SOCS1 partially reversed these levels and pathways. Conclusion miR-155-5p appears to be involved in regulating the inflammatory response in TI-stimulated HaCaT cells by targeting SOCS1, offering a potential mechanistic explanation for the inflammatory dysregulation observed in clinically suspected ACD.