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Updated: Aug 19, 2026
Culturing of Human Nasal Epithelial Cells at the Air Liquid Interface
Published on: October 8, 2013
Lung mucin production is stimulated by the air pollutant residual oil fly ash
M Longphre1, D Li, J Li
1Department of Anatomy and Cardiovascular Research Institute, University of California, San Francisco 94143, USA.
Abstract:
Human and animal exposure to particulate air pollution is correlated with airway mucus hypersecretion and increased susceptibility to infection. Seeking clues to the mechanisms underlying this pathology, we examined the effect of the particulate air pollutant residual oil fly ash (ROFA) on production of the major component of mucus, mucin, and the major antibacterial protein of the respiratory tract, lysozyme. We found that following in vitro exposure to ROFA, epithelial cells showed an increase in mucin (MUC5AC) and lysozyme (LYS) steady state mRNA. This upregulation was controlled at least partly at the level of transcription as shown by reporter assays. Experiments testing the ability of the major components of ROFA to mimic these effects showed that vanadium, a metal making up 18.8% by weight, accounted for the bulk of the response. A screen of signaling inhibitors showed that MUC5AC and LYS induction by ROFA are mediated by dissimilar signaling pathways, both of which are, however, phosphotyrosine dependent. Recognizing that the ROFA constituent vanadium is a potent tyrosine phosphatase inhibitor and that mucin induction by pathogens is phophotyrosine dependent, we suggest that vanadium-containing air pollutants trigger disease-like conditions by unmasking phosphorylation-dependent pathogen resistance pathways.
Insights
Particulate air pollution, like residual oil fly ash (ROFA), increases mucus and lysozyme production in airway cells. Vanadium in ROFA drives this response, potentially by affecting cell signaling pathways.
Area of Science:
- Environmental Health
- Cell Biology
- Toxicology
Background:
- Particulate air pollution is linked to respiratory issues like excess mucus and infection susceptibility.
- Residual oil fly ash (ROFA) is a significant air pollutant with unknown effects on respiratory defenses.
Purpose of the Study:
- To investigate how ROFA affects the production of mucin (MUC5AC) and lysozyme (LYS) in epithelial cells.
- To identify the specific components and signaling pathways involved in ROFA-induced responses.
Main Methods:
- In vitro exposure of epithelial cells to ROFA.
- Measurement of MUC5AC and LYS mRNA levels.
- Reporter assays to assess transcriptional regulation.
- Testing individual ROFA components, particularly vanadium.
- Screening of signaling inhibitors.
Main Results:
- ROFA exposure increased MUC5AC and LYS mRNA steady state levels in epithelial cells.
- Upregulation was partly controlled at the transcriptional level.
- Vanadium was identified as the primary component responsible for the observed effects.
- Distinct, yet phosphotyrosine-dependent, signaling pathways mediated MUC5AC and LYS induction.
Conclusions:
- Vanadium-containing air pollutants, like ROFA, may induce disease-like conditions by interfering with normal cellular defense mechanisms.
- The findings suggest a mechanism where pollutants unmask pathogen resistance pathways through tyrosine phosphatase inhibition.
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