Bronchial epithelial barrier

The bronchial epithelial barrier is not a single molecule or classical therapeutic target, but rather a multicellular, structural, and functional unit formed by epithelial cells lining the bronchi in the airways[1][3][5]. This barrier includes several types of epithelial cells—primarily multiciliated, secretory (goblet), and undifferentiated cells—organized in a pseudostratified layer resting on basal cells with regenerative potential[1][5]. Key features include intercellular junction complexes: tight junctions (claudins, occludins, JAMs), adherens junctions (mainly E-cadherin), and desmosomes, which collectively regulate permeability and maintain structural integrity[4][6]. The bronchial epithelial barrier provides a first line of defense by producing mucus (mainly via MUC5AC and MUC5B mucins) that traps inhaled pathogens and particles, facilitating their clearance by ciliary movement[1][5]. It also regulates immune responses, interacting with innate immune mediators and contributing to host defense through secretion of defensins, IgA, and other protective molecules[1]. Dysfunction or injury of this barrier is implicated in diseases such as asthma and COPD, where increased permeability, loss of cellular junctions, dysregulated repair, and altered epithelial differentiation lead to enhanced susceptibility to infection, chronic inflammation, tissue remodeling, and impaired mucociliary clearance[1][4][5][6]. Because this is a structural barrier rather than a discrete gene, protein, or druggable target, it is generally not considered a direct therapeutic target in drug discovery, but rather a critical element in respiratory physiology and pathology, and a focus for translational research strategies aiming to enhance epithelial repair or reduce barrier disruption in disease[5].

Other names

Airway epithelial barrierRespiratory epithelial barrierAirway mucosal barrier