Bioaerosols and Airway Diseases: Mechanisms of Epithelial Dysfunction, Immune Activation, and Strategies for Exposure Mitigation

Abstract

Bioaerosols-airborne particles of biological origin such as bacteria, fungi, viruses, and allergens-are increasingly recognized as critical environmental factors in the pathogenesis of airway diseases, particularly asthma. This article provides current understanding of how bioaerosols interact with the airway epithelium to initiate acute immune responses, promote chronic inflammation, and drive airway remodeling. Key mechanisms include disruption of mucociliary clearance, activation of innate immune receptors such as TLRs and PRRs, and the role of surfactant proteins SP-A and SP-D in modulating allergic inflammation. Chronic exposure leads to cytokine-mediated fibrosis and smooth muscle hypertrophy, contributing to steroid-resistant asthma. Genetic polymorphisms, especially in innate immunity genes like TLR2, TLR4, and CD14, influence individual susceptibility. The complexity of bioaerosol composition, coupled with environmental variability and lack of standardized exposure thresholds, presents challenges for effective monitoring. However, emerging strategies such as source control, improved ventilation, HEPA filtration, UV disinfection, and real-time airborne pathogen detection offer promising avenues for exposure mitigation. This comprehensive review underscores the need for interdisciplinary approaches to better understand and manage bioaerosol-related respiratory health risks.

Keywords: Airway disease; Airway epithelium; Allergic inflammation; Allergy; Asthma; Bio-aerosols; Genetic polymorphism; Immune activation; Innate immune response; Mucociliary clearance; Toll-like receptor.

Figure 1:

Circular Systems Map Illustrating Epithelial, Immune, and Genetic Interactions in Bioaerosol-Induced Asthma.