Evidence map›Paper›PMID 30804419›Full record

ArticleMucosal immunology2019

The IFN-γ-p38, ERK kinase axis exacerbates neutrophilic chronic rhinosinusitis by inducing the epithelial-to-mesenchymal transition.

Mingyu Lee, Dae Woo Kim, Roza Khalmuratova, Seung-Hyun Shin, Yong-Min Kim, Doo Hee Han, Hyun-Jik Kim, Dong-Young Kim, Chae-Seo Rhee, Jong-Wan Park and 1 more

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In one paragraph

Article in Mucosal immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
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  5. Review
  6. Neutrophil Killing ofJournal of innate immunity · 2026
    Article
  7. [Advances in the pathogenesis and treatment of neutrophils in chronic sinusitis].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2025
    Review
  8. Article
  9. IL-8 promotes pyroptosis through ERK pathway and mediates glucocorticoid resistance in chronic rhinosinusitis with nasal polyps.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  10. [Research progress of type 2 inflammation-related tissue remodeling in nasal polyps].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2024
    Review
  11. Epithelial-Mesenchymal Transition in Chronic Rhinosinusitis.Journal of rhinology : official journal of the Korean Rhinologic Society · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. [The expression and significance of Piezo1 in chronic rhinosinusitis with nasal polyps].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2023
    Article
  17. Article
  18. Review
  19. Article
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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

11 authors at 5 institutions in 1 country.

Mingyu LeeObstructive Upper airway Research (OUaR) Laboratory, Department of Pharmacology, Seoul National University College of Medicine, Seoul, Korea.
Dae Woo KimDepartment of Otorhinolaryngology-Head and Neck Surgery, Boramae Medical Center, Seoul, Korea.
Roza KhalmuratovaObstructive Upper airway Research (OUaR) Laboratory, Department of Pharmacology, Seoul National University College of Medicine, Seoul, Korea.
Seung-Hyun ShinDepartment of Biomedical Sciences, Seoul National University Graduate School, Seoul, Korea.
Yong-Min KimDepartment of Otorhinolaryngology-Head and Neck Surgery, Chungnam National University Hospital, Daejun, Korea.
Doo Hee HanDepartment of Otorhinolaryngology-Head and Neck Surgery, Seoul National University Hospital, Seoul, Korea.
Hyun-Jik KimDepartment of Otorhinolaryngology-Head and Neck Surgery, Seoul National University Hospital, Seoul, Korea.
Dong-Young KimDepartment of Otorhinolaryngology-Head and Neck Surgery, Seoul National University Hospital, Seoul, Korea.
Chae-Seo RheeDepartment of Otorhinolaryngology-Head and Neck Surgery, Seoul National University Bundang Hospital, Seongnam, Korea.
Jong-Wan ParkObstructive Upper airway Research (OUaR) Laboratory, Department of Pharmacology, Seoul National University College of Medicine, Seoul, Korea.
Hyun-Woo ShinObstructive Upper airway Research (OUaR) Laboratory, Department of Pharmacology, Seoul National University College of Medicine, Seoul, Korea. charlie@snu.ac.kr.
Seoul National University · KRSeoul National University Hospital · KRSNUH SMG-SNU Boramae Medical Center · KRChungnam National University Hospital · KRSeoul National University Bundang Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic rhinosinusitis (CRS) is a heterogeneous and multifactorial inflammatory disease characterized by involvement of diverse types of inflammatory cells. Asian CRS patients frequently show infiltration of neutrophils and an elevated level of interferon (IFN)-γ; by contrast, western patients exhibit eosinophil infiltration and enhanced levels of Th2-related cytokines. Neutrophilia in tissues decreases sensitivity to corticosteroids, but the mechanisms underlying the progression of neutrophilic CRS are unclear. In this study, we investigated the role of IFN-γ in CRS patients with marked neutrophil infiltration. We report that the IFN-γ level is upregulated in the tissues of these patients, particularly those with non-eosinophilic nasal polyps. The level of IFN-γ was significantly correlated with markers of the epithelial-to-mesenchymal transition (EMT). We further demonstrated that IFN-γ induced the EMT via the p38 and extracellular signal-regulated kinase (ERK) pathways in a manner distinct from the hypoxia-inducible factor (HIF)-1α, SMAD, and NF-κB signaling pathways. In a murine nasal polyp (NP) model, blocking the p38 and ERK signaling pathways prevented NP formation and chemotactic cytokine secretion by neutrophils but not eosinophils. Taken together, our results suggest that IFN-γ can induce the EMT in nasal epithelial cells, and thus blocking the p38 and ERK pathways could be an effective therapeutic strategy against neutrophil-dominant CRS.

Indexed as

AdultAgedAnimalsCells, CulturedChronic DiseaseDisease Models, AnimalEpithelial-Mesenchymal TransitionExtracellular Signal-Regulated MAP KinasesFemaleHumansInterferon-gammaMaleMiceMice, Inbred BALB CMiddle AgedNeutrophilsExtracellular Signal-Regulated MAP KinasesInterferon-gammap38 Mitogen-Activated Protein Kinases

Identifiers

PMID30804419
OpenAlexW2917056797

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.