Air pollution and microplastic as modifiers of epithelial injury and repair in models of acute, chronic, and allergic airway inflammation.

The toxic effects of air pollutants on the airway epithelium are associated with oxidative stress, a pro-inflammatory response, and impaired innate immune responses. The chronic exposure to noxious factors leads to cumulative damage to the alveolar compartment, reduced diffusion capacity, and impaired lung function. This study aimed to investigate the biological responses of bronchial epithelial cells exposed to PM2.5 and microplastic, following prior induction of acute, chronic, and allergic epithelial injury. Primary, normal bronchial epithelial cells were cultivated in air-liquid interface (ALI) in models of normal, acute (lipopolysaccharide (LPS) treated), chronic (cigarette smoke extract (CSE) treated for 14 days), and allergic (house dust mite (HDM) + IL-13 treated for 3 days). Simultaneously, cells were divided into two groups: uninjured or physically injured by a scratch. Cells were then stimulated with microplastic fibres (200 μg/cm2) and PM2.5 (50 μg per insert) applied to the top of the epithelial cell layer for 48 h. Combined exposure to PM2.5 and microplastics induced profound cytotoxic effects across all models. Mechanical injury modulated inflammatory responses in a model-dependent manner, with the most pronounced dysregulation observed in allergically primed epithelial cells. In control and LPS-stimulated cultures, co-exposure to PM2.5 and microplastics significantly disrupted epithelial barrier integrity. PM2.5 and microplastic exposure were associated with increased TGF-β and EGFR expression across several injury models, with a tendency toward enhanced TGF-β signalling in secretory epithelial cells under chronic and allergic conditions, largely independent of mechanical injury. Overall, pollutant-induced responses varied according to the underlying epithelial injury state. Atmospheric pollutants influenced epithelial immune response, contributing to airway epithelial injury and affecting regenerative capacity, particularly when cellular biology was additionally compromised by bacterial, tobacco or allergic stimuli.