Particulate Matter (PM2.5) Exposure Accelerates Airway Remodeling via Activation of the NLRP3 Inflammasome in Moderate-to-Severe Allergic Rhinitis and Asthma

Research Paper | 2026 | Volume 1 | Issue 01 | Page 31-35

Dr. Arbas Mulla, Department of Respiratory Medicine, Dubai Medical College, UAE

Particulate Matter (PM2.5) Exposure Accelerates Airway Remodeling via Activation of the NL

Download 5) EXPOSURE ACCELERATES AIRWAY REMODELING VIA ACTIVATION OF THE NL • 198KB

ABSTRACT BACKGROUND: Epidemiological evidence suggests a strong correlation between fine particulate matter (PM2.5) exposure and the exacerbation of chronic respiratory conditions. However, the precise molecular mechanisms by which PM2.5 drives structural changes in the airways of patients with comorbid Allergic Rhinitis (AR) and Asthma—a phenomenon known as the "united airway disease"—remain poorly characterized. This study investigates the hypothesis that PM2.5 exposure accelerates airway remodeling by activating the NLRP3 inflammasome pathway. METHODS: A murine model of combined AR and asthma was exposed to concentrated ambient PM2.5 (500 μg/m³) over a 4-week period. Airway remodeling was assessed via histological quantification of subepithelial fibrosis, smooth muscle hypertrophy, and goblet cell hyperplasia. The activation of the NLRP3 inflammasome (NLRP3, ASC, and Caspase-1) and downstream pro-inflammatory cytokines (IL-1β and IL-18) were measured in nasal and bronchial mucosa using RT-qPCR, Western blotting, and immunohistochemistry. The role of the NLRP3 pathway was further validated using an NLRP3-specific inhibitor (MCC950). RESULTS: PM2.5 exposure significantly intensified airway remodeling, characterized by enhanced collagen deposition and smooth muscle thickening, compared to non-exposed AR-asthma controls. This structural deterioration was associated with marked upregulation of the NLRP3 inflammasome complex and elevated secretion of IL-1β and IL-18 in both nasal and bronchial tissues. Treatment with MCC950 effectively attenuated PM2.5-induced structural remodeling and reduced pro-inflammatory cytokine levels, confirming the causative role of the NLRP3 inflammasome. CONCLUSION: PM2.5 exposure acts as a potent molecular trigger that accelerates airway remodeling in AR-asthma models via the activation of the NLRP3 inflammasome. Targeting this pathway may provide a novel therapeutic strategy to mitigate respiratory decline in patients living in polluted environments. KEYWORDS: PM2.5, Allergic Rhinitis, Asthma, Airway Remodeling, NLRP3 Inflammasome, IL-1β, United Airway Disease. Particulate Matter (PM2.5) Exposure Accelerates Airway Remodeling via Activation of the NLRP3 Inflammasome in Moderate-to-Severe Allergic Rhinitis and Asthma