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pubmed:abstractText |
Asthma is a chronic airway inflammatory disease characterized by an imbalance in both Th1 and Th2 cytokines. Exhaled nitric oxide (NO) is elevated in asthma, and is a potentially useful non-invasive marker of airway inflammation. However, the origin and underlying mechanisms of intersubject variability of exhaled NO are not yet fully understood. We have previously described NO gas phase release from normal human bronchial epithelial cells (NHBEs, tracheal origin). However, smaller airways are the major site of morbidity in asthma. We hypothesized that IL-13 or cytomix (IL-1beta, TNF-alpha, and IFN-gamma) stimulation of differentiated small airway epithelial cells (SAECs, generation 10-12) and A549 cells (model cell line of alveolar type II cells) in culture would enhance NO gas phase release.
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