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
AUTHORS (8)
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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