Wood Smoke Particles Stimulate MUC5AC Overproduction by Human Bronchial Epithelial Cells Through TRPA1 and EGFR Signaling

0301 basic medicine Inhalation Exposure Glycogen Synthase Kinase 3 beta Bronchi Epithelial Cells Mucin 5AC Wood p38 Mitogen-Activated Protein Kinases Up-Regulation 3. Good health ErbB Receptors Mice, Inbred C57BL 03 medical and health sciences 13. Climate action Smoke 11. Sustainability Animals Humans TRPA1 Cation Channel Cells, Cultured Signal Transduction
DOI: 10.1093/toxsci/kfaa006 Publication Date: 2020-01-10T20:10:32Z
ABSTRACT
Abstract Mucus hypersecretion is a pathological feature of acute inflammatory and chronic obstructive pulmonary diseases. Exposure to air pollutants can be cause mucus overproduction, but mechanisms by which different forms elicit this response are not fully understood. In study, particulate matter (PM) generated from burning pine wood other types biomass was used determine these PM stimulate mucin gene expression secretion primary human bronchial epithelial cells (HBECs). Biomass < 2.5 μm several fuels stimulated the gel-forming glycoprotein MUC5AC HBECs. Muc5ac induction also observed in mouse airways following subacute oropharyngeal delivery smoke PM. HBECs, induced transient receptor potential ankyrin-1 (TRPA1) agonists’ coniferaldehyde, component PM, allyl isothiocyanate, attenuated TRPA1 antagonist. Additionally, inhibition epidermal growth factor (EGFR/ErbB1) EGFR signaling partners p38 MAPK GSK3β prevented overexpression. Collectively, our results suggest that activation EGFR, paired with alterations activity, plays major role overproduction exposed These reveal specific processes for how may impact respiratory system highlight avenues therapeutic manipulation lung diseases affected pollutants.
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