Evidence map›Paper›PMID 31020341›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2019

Critical role of interleukin-23 in development of asthma promoted by cigarette smoke.

Hyun Seung Lee, Da-Eun Park, Ji-Won Lee, Hoe-Na Kim, Woo-Jung Song, Heung-Woo Park, Sang-Heon Cho

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Role of mTOR in the Development of Asthma in Mice With Cigarette Smoke-Induced Cellular Senescence.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022
    Article
  8. Article
  9. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Hyun Seung LeeInstitute of Allergy and Clinical Immunology, Medical Research Center, Seoul National University, 101 Daehak-ro, Jongno-gu, Seoul, 110-744, South Korea. gentlehood79@hanmail.net.ORCID http://orcid.org/0000-0002-4599-8527
Da-Eun ParkInstitute of Allergy and Clinical Immunology, Medical Research Center, Seoul National University, 101 Daehak-ro, Jongno-gu, Seoul, 110-744, South Korea.
Ji-Won LeeDivision of Allergy and Clinical Immunology, Department of Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Republic of Korea.
Hoe-Na KimInstitute of Allergy and Clinical Immunology, Medical Research Center, Seoul National University, 101 Daehak-ro, Jongno-gu, Seoul, 110-744, South Korea.
Woo-Jung SongDivision of Allergy and Clinical Immunology, Department of Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Republic of Korea.
Heung-Woo ParkDepartment of Internal Medicine, College of Medicine, Seoul National University, Seoul, Republic of Korea.
Sang-Heon ChoInstitute of Allergy and Clinical Immunology, Medical Research Center, Seoul National University, 101 Daehak-ro, Jongno-gu, Seoul, 110-744, South Korea.
Seoul National University · KRAsan Medical Center · KRSeoul National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been recently reported that cigarette smoke exposure during allergen sensitization facilitates the development of allergic asthma; however, the underlying mechanisms remain elusive. We evaluated the role of interleukin (IL-23) in a cigarette smoke extract (CSE)-induced Dermatophagoides pteronyssinus (Dp)-allergic asthma mouse model. BALB/c mice were exposed to CSE during allergen sensitization period. Anti-IL-23p19 or IL-23R antibody was administered during the sensitization period. And we evaluated several immunological responses. The expression of IL-23 and IL-23 receptor (IL-23R) was examined in lung tissue. IL-23 and IL-23R expression was increased in the airway epithelium of Dp/CSE co-administered mice. CSE administration during the sensitization promoted Dp-allergic sensitization and the development of asthma phenotypes. Additionally, the proportion of innate lymphoid type 2 cells (ILC2) was also increased by CSE and Dp co-instillation. Anti-IL-23 or IL-23R antibody treatment during allergen sensitization significantly diminished phenotypes of allergic asthma and the ILC2 population. The levels of IL-33 and thymic stromal lymphopoietin (TSLP) were also significantly reduced by anti-IL-23 or IL-23R antibody treatment. IL-23 may thus play a significant role in cigarette smoke-induced allergic sensitization and asthma development. Clinically, the increase in allergen sensitization due to cigarette exposure causes onset of asthma, and IL-23 may be important in this mechanism. KEY MESSAGES: IL-23 and IL-23R expression was increased in the lung epithelium of Dp and CSE co-exposed mice during sensitization period. The population of ILC2s was increased in Dp and CSE co-exposed mice during sensitization period. Anti-IL23 or IL-23R antibody treatment with co-administration of CSE and HDM during sensitization period significantly suppresses ILC2. In vitro, IL-23 blockade in Dp and CSE-stimulated epithelial cells suppressed IL-13 expression in ILC2.

Indexed as

AnimalsAntibodiesAsthmaBronchial HyperreactivityCigarette SmokingCytokinesDendritic CellsDermatophagoides pteronyssinusEpithelial CellsEpitheliumFemaleImmunity, InnateImmunizationInterleukin-13Interleukin-23Interleukin-33AntibodiesCytokinesInterleukin-13Interleukin-23interleukin-23 receptor, mouseInterleukin-33Receptors, InterleukinThymic Stromal LymphopoietinCigarette smokeHouse dust miteIL-23IL-23 receptor

Identifiers

PMID31020341
OpenAlexW2941536706

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.