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The bronchial epithelial barrier function is a fundamental component of the lung's innate defense system, composed of a specialized layer of epithelial cells that are interconnected by apical junctional complexes (Georas & Rezaee, 2014, J Allergy Clin Immunol). These complexes, which include tight junctions (comprising proteins like claudins, occludin, and zonula occludens-1) and adherens junctions (comprising E-cadherin), regulate paracellular permeability and prevent the entry of environmental stressors such as allergens, pathogens, and pollutants (Heijink et al., 2020, Eur Respir Rev). In chronic respiratory conditions like asthma and COPD, this barrier is frequently compromised, leading to increased susceptibility to infections and the release of pro-inflammatory alarmins like TSLP and IL-33 (Steelant et al., 2016, J Allergy Clin Immunol). Therapeutic approaches targeting this barrier often involve the use of inhaled corticosteroids, which have been shown to enhance the expression of junctional proteins and improve barrier integrity (Ganesan et al., 2013, Am J Physiol Lung Cell Mol Physiol). Additionally, biological therapies that inhibit cytokines like IL-13 or TSLP help to prevent the breakdown of these junctions and reduce airway hyperresponsiveness (Gonem et al., 2014, Lancet Respir Med). Restoring the bronchial epithelial barrier is considered a key strategy for achieving long-term disease control and preventing exacerbations in patients with chronic airway diseases.
Enhancement of apical junctional complex protein expression and inhibition of barrier-disrupting inflammatory cytokines.
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