From triggers to asthma: a narrative review on epithelium dysfunction

Area of Science:

• Respiratory Medicine
• Immunology
• Cell Biology

Background:

• The airway epithelium is a key player in asthma pathogenesis.
• It orchestrates inflammatory, immune, and regenerative responses to various triggers.
• Its role extends beyond barrier function to actively modulating immune responses.

Purpose of the Study:

• To review the pathophysiology and functions of the airway epithelium in asthma.
• To elucidate the role of epithelial damage by diverse triggers in asthma development and exacerbations.
• To highlight the multifaceted impact of allergens, viruses, and pollutants on respiratory epithelium.

Main Methods:

• Literature review of existing research on airway epithelium in asthma.
• Analysis of the mechanisms by which pollen, pollutants, and viruses affect the airway epithelium.
• Examination of epithelial cell-derived mediators and their downstream effects.

Main Results:

• Pollen, pollutants, and viruses activate airway epithelial cells to release cytokines (alarmins).
• Epithelial damage leads to barrier dysfunction, inflammation, and immune activation (including Th2 responses).
• Epithelial triggers contribute to airway smooth muscle remodeling and hyperreactivity.

Conclusions:

• The airway epithelium is central to asthma pathophysiology, not just a passive barrier.
• Damage and activation of the airway epithelium by environmental factors are critical in asthma development and persistence.
• Understanding epithelial responses is vital for developing new asthma therapies.