{'fraction_non_alphanumeric': 0.03387220939183987, 'fraction_numerical': 0.01308698999230177, 'mean_word_length': 5.467661691542289, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Enhanced release of thromboxane A2 after exposure of human airway epithelial cells to meconium

Meconium aspiration syndrome (MAS) is a cause of significant morbidity and mortality in the perinatal period. Despite the clinical relevance of MAS, its pathogenesis is poorly understood. Epithelial cell‐derived prostanoids are involved in the regulation of several cellular functions within the lung, including the control of tone and reactivity of airway and vascular smooth muscle. In this study, we evaluated whether exposure to meconium affects the metabolic function of human airway epithelial cells. Monolayers of A549 cells, a transformed human epithelial cell line, were incubated with various concentrations of meconium. Control cells were incubated with serum‐free medium in a similar manner. The supernatant fluid was removed at various time points and assayed for thromboxane A2 (TXA2) production. The latter was accomplished by measuring its immediate and stable metabolite thromboxane B2, using an enzyme‐linked immunosorbent assay (ELISA). In selected experiments, the modulatory effects of indomethacin (10− 6 M), dexamethasone (10− 6 M), and L‐nitroarginine methyl ester (L‐NAME, 10− 6 M) on TXA2 production were evaluated. Results were expressed in terms of pg/mg protein (mean ± SE).