Evidence map›Paper›PMID 32269574›Full record

ReviewFrontiers in immunology2020

Inactivation of FOXA2 by Respiratory Bacterial Pathogens and Dysregulation of Pulmonary Mucus Homeostasis.

Woosuk Choi, Shawn Choe, Gee W Lau

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Frontiers in immunology · 2026
    Article
  5. Article
  6. Article
  7. Research Progress on the Mechanisms of High Mucus Secretion in the Airway: A Scoping Review.International journal of chronic obstructive pulmonary disease · 2026
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Journal of fungi (Basel, Switzerland) · 2023
    Article
  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

3 authors at 1 institution in 1 country.

Woosuk ChoiDepartment of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, IL, United States.
Shawn ChoeDepartment of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, IL, United States.
Gee W LauDepartment of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, IL, United States.
University of Illinois Urbana-Champaign · US

Funding

Controlling bactermic pneumococcal pneumonia with synthetic dominant-negative competence peptidesR01HL142626 · NHLBI · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI LAU, GEE W, TALGAN, YIFTAH · 2019 to 2022
$2.0M
Mechanisms of Pseudomonas Resistance to Membrane Permeabilization by SP-AR01HL090699 · NHLBI · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI LAU, GEE W · 2009 to 2012
$1.6M
NHLBI NIH HHS R01 HL090699NHLBI NIH HHS R01 HL142626
6 · The paper itself

Abstract

Forkhead box (FOX) proteins are transcriptional factors that regulate various cellular processes. This minireview provides an overview of FOXA2 functions, with a special emphasis on the regulation airway mucus homeostasis in both healthy and diseased lungs. FOXA2 plays crucial roles during lung morphogenesis, surfactant protein production, goblet cell differentiation and mucin expression. In healthy airways, FOXA2 exerts a tight control over goblet cell development and mucin biosynthesis. However, in diseased airways, microbial infections and proinflammatory responses deplete FOXA2 expression, resulting in uncontrolled goblet cell hyperplasia and metaplasia, mucus hypersecretion, and impaired mucociliary clearance of pathogens. Furthermore, accumulated mucus clogs the airways and creates a niche environment for persistent microbial colonization and infection, leading to acute exacerbation and deterioration of pulmonary function in patients with chronic lung diseases. Various studies have shown that FOXA2 inhibition is mediated through induction of antagonistic EGFR and IL-13R-STAT6 signaling pathways as well as through posttranslational modifications induced by microbial infections. An improved understanding of how bacterial pathogens inactivate FOXA2 may pave the way for developing therapeutics that preserve the protein's function, which in turn, will improve the mucus status and mucociliary clearance of pathogens, reduce microbial-mediated acute exacerbation and restore lung function in patients with chronic lung diseases.

Indexed as

AnimalsErbB ReceptorsHepatocyte Nuclear Factor 3-betaHomeostasisHumansLungMiceMucous MembraneReceptors, Interleukin-13Respiratory Tract InfectionsSignal TransductionSTAT6 Transcription FactorEGFR protein, humanErbB ReceptorsFOXA2 protein, humanHepatocyte Nuclear Factor 3-betaReceptors, Interleukin-13STAT6 Transcription Factorchronic lung diseasesEGFRFOXA2MUC5ACMUC5Bmucociliary clearancemucus homeostasisSTAT6

Identifiers

PMID32269574
PMCPMC7109298
OpenAlexW3014061138

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.