Mitochondrial ROS activate interleukin-1β expression in allergic rhinitis

Area of Science:

• Immunology
• Pathophysiology

Background:

• Allergic rhinitis (AR) is a prevalent inflammatory condition of the nasal mucosa, often IgE-mediated.
• Interleukin-1β (IL-1β) is implicated in allergic asthma pathogenesis.
• The role of IL-1β in AR pathogenesis requires further investigation.

Purpose of the Study:

• To investigate the potential role of IL-1β in the pathogenesis of allergic rhinitis.
• To assess the relationship between IL-1β, mitochondrial reactive oxygen species (ROS), and IL-17 in AR patients.

Main Methods:

• Enrolled 45 patients diagnosed with AR.
• Measured IL-1β expression in peripheral blood mononuclear cells (PBMCs).
• Assessed the requirement of mitochondrial ROS and NLRP3 for IL-1β synthesis.

Main Results:

• Patients with AR exhibited increased IL-1β expression in PBMCs.
• Mitochondrial ROS and NLRP3 were essential for IL-1β synthesis in monocytes/macrophages and PBMCs.
• Elevated levels of IL-1β and IL-17 were observed in AR patients and were positively correlated.

Conclusions:

• Mitochondrial ROS may upregulate IL-1β expression in AR.
• Increased IL-1β potentially influences IL-17 production, contributing to AR pathogenesis.
• IL-1β is suggested to play a significant role in the inflammatory processes of allergic rhinitis.