Abstract
Airway epithelial cells lie at the interface between a host and its environment, representing the first line of defense against pathogens. In addition to its role as a protective barrier, the airway epithelium can activate underlying dendritic cells, thereby initiating and prolonging airway inflammation. Furthermore, alterations in epithelial ion transport mechanisms can modify many aspects of epithelial signaling, mucus properties, bacterial defenses, and induction of immune responses. IL‐6 is a proinflammatory cytokine produced mainly by cells of the innate immune system and is increased in a variety of pulmonary diseases, though its role(s) remain unclear. The objective of our research is to determine the mechanism(s) by which the airway epithelium drives the immunopathology of allergic asthma and to clarify the relationship(s) between the epithelium and IL‐6 in the pathogenesis of asthma. Normal Human Bronchial Epithelial (NHBE)(Lonza Walkersville) were grown on collagen‐coated transwell inserts and cultured at air‐liquid interface (ALI) for ~20d to achieve full differentiation. Transepithelial resistance (TER) was monitored, and upon reaching 350‐500 Ω, the cells were treated with house dust mite allergen (HDM, 50 or 100 ug/mL; Greer Laboratories) for 24 h. IL‐6 cytokine production was measured via ELISA (R&D Systems). IL‐6 production increased in a dose‐dependent manner in HDM‐treated cultures (50 ug/ml HDM: 878+/‐235 pg/mL, or 142% increase, and for 100 ug/mL of HDM: 1325+/‐18.7 pg/mL, or 215% increase, p=0.04) as compared to sham treatment groups (618+/‐433 pg/mL). Our data indicate that bronchial epithelial cells may drive allergic asthma via production of IL‐6. Our ongoing studies seek to determine the relationship(s) between the airway epithelium, IL‐6 production, and other aspects of epithelial dysfunction in asthma pathogenesis, including dysregulated mucus production and epithelial ion transport.
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