Mitochondrial ROS activate interleukin‑1β expression in allergic rhinitis

Abstract

Allergic rhinitis (AR) is the most common cause of inflammation of the nasal mucosa. It is also the most common form of non‑infectious rhinitis associated with an immunoglobulin E (IgE)‑mediated immune response against allergens. Previous studies have indicated that interleukin‑1β (IL‑1β) has a pathological role in the development of allergic asthma. The present study was designed to assess whether IL‑1β participates in the pathogenesis of AR. A total of 45 patients with AR were enrolled in the present study and were identified to have increased IL‑1β expression expressed by peripheral blood mononuclear cells (PBMCs), and the mitochondrial reactive oxygen species (ROS) and NLRP3 are required for IL‑1β synthesis in monocytes/macrophages and PBMCs from patients with AR. The levels of IL‑1β and interleukin‑17 (IL‑17) were increased in patients with AR and were positively correlated with each other. The results of the present study suggested that patients with AR have raised mitochondrial ROS levels, which may upregulate the expression of IL‑1β, affecting IL‑17‑production and serving a role in the pathogenesis of AR.