IL-2 regulates oral mucosa inflammation through inducing endoplasmic reticulum stress and activating the NF-κB pathway

Objective: The molecular mechanism underlying oral mucosa inflammation remains unknown. Aim: The aim of our study is to explore the influence of interleukin-2 (IL-2) in regulating oral mucosa viability and inflammation response. Methods: Oral mucosa epithelium was treated with IL-2. Cell viability and death were determined via 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromidefo (MTT) assay and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, respectively. Inflammation response was measured via enzyme-linked immunosorbent assay (ELISA), and quantitative polymerase chain reaction (qPCR). Western blot and immunofluorescence were used to verify the alterations of nuclear factor-kappa B (NF-kappa B) pathway. Results: IL-2 treatment induced a loss of cell viability in oral mucosa. Besides, inflammatory factors transcription and expression were significantly elevated in response to IL-2 treatment. In addition, oxidative stress and cell apoptosis were also augmented by IL-2 treatment. Mechanistically, IL-2 treatment was associated with an activation of the NF-kappa B pathway. Inhibition of NF-kappa B pathway could abolish the promotive effects exerted by IL-2 on oral mucosa death and inflammation response. Conclusion: Taken together, our results demonstrated that IL-2 treatment activated NF-kappa B pathway and then promoted oral mucosa inflammation, leading to intracellular oxidative stress and cell apoptosis.