Evidence map›Paper›PMID 31944254›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2020

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

Tosifa A Memon, Nam D Nguyen, Katherine L Burrell, Abigail F Scott, Marysol Almestica-Roberts, Emmanuel Rapp, Cassandra E Deering-Rice, Christopher A Reilly

Open access · greenAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Air pollution-induced airway epithelial barrier dysfunction in COPD: a narrative review of mechanisms and therapeutic implications.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Research Progress on TRPA1 in Diseases.The Journal of membrane biology · 2023
    Review
  9. Article
  10. The Effects of Wildfire Smoke on Asthma and Allergy.Current allergy and asthma reports · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. The Effects and Pathogenesis of PM2.5 and Its Components on Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023
    Review
  15. Review
  16. Article
  17. Article
  18. Role of air pollutants in airway epithelial barrier dysfunction in asthma and COPD.European respiratory review : an official journal of the European Respiratory Society · 2022
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Tosifa A MemonDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Nam D NguyenDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Katherine L BurrellDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Abigail F ScottDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Marysol Almestica-RobertsDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Emmanuel RappDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Cassandra E Deering-RiceDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Christopher A ReillyDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
University of Utah · US

Funding

TRP Channels and Air PollutionR01ES017431 · NIEHS · UNIVERSITY OF UTAH · PI REILLY, CHRISTOPHER A · 2009 to 2024
$5.3M
Pharmacogenomic and Metabolic Optimization of Glucocorticoid Therapy for AsthmaR01GM121648 · NIGMS · UNIVERSITY OF UTAH · PI REILLY, CHRISTOPHER A · 2017 to 2020
$2.5M
Pulmonary Epithelial TRPV3 and Wood Smoke InjuryR01ES027015 · NIEHS · UNIVERSITY OF UTAH · PI REILLY, CHRISTOPHER A · 2017 to 2021
$1.7M
NCRR Confocal ProposalS10RR024761 · NCRR · UNIVERSITY OF UTAH · PI RODESCH, CHRISTOPHER K · 2008 to 2008
$475k
NCRR NIH HHS S10 RR024761NIEHS NIH HHS R01 ES017431NIEHS NIH HHS R01 ES027015NIGMS NIH HHS R01 GM121648
6 · The paper itself

Abstract

Mucus hypersecretion is a pathological feature of acute inflammatory and chronic obstructive pulmonary diseases. Exposure to air pollutants can be a cause of pathological mucus overproduction, but mechanisms by which different forms of air pollutants elicit this response are not fully understood. In this study, particulate matter (PM) generated from burning pine wood and other types of biomass was used to determine mechanisms by which these forms of PM stimulate mucin gene expression and secretion by primary human bronchial epithelial cells (HBECs). Biomass PM < 2.5 μm generated from pine wood and several other fuels stimulated the expression and secretion of the gel-forming glycoprotein MUC5AC by HBECs. Muc5ac gene induction was also observed in mouse airways following subacute oropharyngeal delivery of pine wood smoke PM. In HBECs, MUC5AC was also induced by the transient receptor potential ankyrin-1 (TRPA1) agonists' coniferaldehyde, a component of pine smoke PM, and allyl isothiocyanate, and was attenuated by a TRPA1 antagonist. Additionally, inhibition of epidermal growth factor receptor (EGFR/ErbB1) and the EGFR signaling partners p38 MAPK and GSK3β also prevented MUC5AC overexpression. Collectively, our results suggest that activation of TRPA1 and EGFR, paired with alterations to p38 MAPK and GSK3β activity, plays a major role in MUC5AC overproduction by bronchial epithelial cells exposed to biomass smoke PM. These results reveal specific processes for how biomass smoke PM may impact the human respiratory system and highlight potential avenues for therapeutic manipulation of lung diseases that are affected by air pollutants.

Indexed as

AnimalsBronchiCells, CulturedEpithelial CellsErbB ReceptorsGlycogen Synthase Kinase 3 betaHumansInhalation ExposureMice, Inbred C57BLMucin 5ACp38 Mitogen-Activated Protein KinasesSignal TransductionSmokeTRPA1 Cation ChannelUp-RegulationWoodEGFR protein, humanErbB ReceptorsGlycogen Synthase Kinase 3 betaGSK3B protein, humanMUC5AC protein, humanMucin 5ACp38 Mitogen-Activated Protein KinasesSmokeTRPA1 Cation ChannelTRPA1 protein, humanEGFRMUC5ACmucinparticulate matterTRPA1wood smoke

Identifiers

PMID31944254
PMCPMC7098379
OpenAlexW3000600603

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.