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

Abstract

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-κB (NF-κB) 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-ĸB pathway. Inhibition of NF-ĸB 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-ĸB pathway and then promoted oral mucosa inflammation, leading to intracellular oxidative stress and cell apoptosis.

Keywords:

• IL-2
• oral mucosa
• inflammation
• NF-ĸB pathway

Disclosure statement

The authors have declared that they have no conflicts of interest.

Data availability statement

All data generated or analyzed during this study are included in this published article.