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• W2083411345 abstract "Mucin overproduction is a hallmark of chronic inflammatory airway diseases, such as asthma, chronic obstructive pulmonary disease, and cystic fibrosis. Excessive production of mucin leads to airway mucus obstruction and contributes to morbidity and mortality in these diseases. The molecular mechanisms underlying mucin overproduction, however, still remain largely unknown. Here, we report that the bacterium P. aeruginosa, an important human respiratory pathogen causing cystic fibrosis, utilizes reactive oxygen species (ROS) to up-regulate MUC5AC mucin expression. Pseudomonas aeruginosa lipopolysaccharide (PA-LPS) induces production of ROS through protein kinase C (PKC)-NADPH oxidase signaling pathway in human epithelial cells. Subsequently, ROS generation by PA-LPS releases transforming growth factor-α (TGF-α), which in turn, leads to up-regulate MUC5AC expression. These findings may bring new insights into the molecular pathogenesis of P. aeruginosa infections and lead to novel therapeutic intervention for inhibiting mucin overproduction in patients with P. aeruginosa infections." @default.
• W2083411345 created "2016-06-24" @default.
• W2083411345 creator A5001969147 @default.
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• W2083411345 date "2008-02-01" @default.
• W2083411345 modified "2023-10-16" @default.
• W2083411345 title "Reactive oxygen species regulate Pseudomonas aeruginosa lipopolysaccharide-induced MUC5AC mucin expression via PKC-NADPH oxidase-ROS-TGF-α signaling pathways in human airway epithelial cells" @default.
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• W2083411345 doi "https://doi.org/10.1016/j.bbrc.2007.11.172" @default.
• W2083411345 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18073139" @default.
• W2083411345 hasPublicationYear "2008" @default.
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