Melatonin reduces IL‐33 and TSLP expression in human nasal epithelial cells by scavenging ROS directly

Abstract

Background Chronic rhinosinusitis (CRS) is a chronic mucosal inflammation of the nasal cavity and sinuses. It is classified into CRS without nasal polyps and CRS with nasal polyps (CRSwNP). CRSwNP has high recurrence, especially CRSwNP with massive eosinophil infiltration which is mediated by type 2 inflammatory response. Melatonin is a hormone secreted by the pineal gland, it has powerful antioxidant and anti‐inflammatory effects in addition to regulating biological rhythms. There are no studies on melatonin for the treatment of CRS, so we aimed to explore whether melatonin could be used for the treatment of CRS. Materials and Methods In this study, we used melatonin to treat a cell model of CRS. Subsequently, MTT assay was performed to examine the cell viability of human nasal epithelial cells (HNEpCs), a reactive oxygen species (ROS) kit to detect ROS production, a malondialdehyde (MDA) kit to detect the MDA content in the cell culture supernatant, and an apoptosis kit and Western blot analysis to detect apoptosis. The expressions of Nrf2, HO‐1, IL‐33, TSLP, and IL‐25 were detected by Western blot analysis. Results Melatonin improved the viability of HNEpCs, reduced lipopolysaccharide‐induced ROS, reduced the MDA content, and inhibited their apoptosis. More importantly, melatonin reduced the expression of IL‐33 and TSLP, an important phenomenon for the treatment of CRSwNP. Conclusion Melatonin protects HNEpCs from damage in inflammation and reduces IL‐33 and TSLP expression of HNEpCs.

Melatonin in food allergy: Mechanism and potential therapy

“…Similarly, melatonin treatment inhibits IL‐33 produced by renal tissues in diabetic kidney disease and contrast‐induced nephropathy 84 . Consistently, a recent study has clarified that melatonin inhibits the release of IL‐33 and TSLP from human nasal epithelial cells (HNEpCs) by scavenging ROS in vitro 85 (Figure 1I), suggesting that melatonin reduces the expression of OX40L in DCs by relieving oxidative stress and inhibiting cytokine production from epithelial cells.…”