Evidence map›Paper›PMID 31072323›Full record

ArticleJournal of translational medicine2019

Interferon gamma induces inflammatory responses through the interaction of CEACAM1 and PI3K in airway epithelial cells.

Yichun Zhu, Dongli Song, Yuanlin Song, Xiangdong Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-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

29 citing papers in PubMed, 35 citations in OpenAlex.

  1. Octreotide Counteracts IFN-γ-Induced Endothelial Inflammation.Journal of biochemical and molecular toxicology · 2026
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  16. CEACAM expression in anFrontiers in immunology · 2023
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  17. SARS-CoV-2 particles promote airway epithelial differentiation and ciliation.Frontiers in bioengineering and biotechnology · 2023
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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

4 authors at 2 institutions in 1 country.

Yichun ZhuZhongshan Hospital Institute of Clinical Science, Shanghai, China.
Dongli SongZhongshan Hospital Institute of Clinical Science, Shanghai, China.
Yuanlin SongDepartment of Respiratory Medicine of Zhongshan Hospital, Fudan University, Shanghai, China.
Xiangdong WangZhongshan Hospital Institute of Clinical Science, Shanghai, China. Xiangdong.wang@clintransmed.org.
Zhongshan Hospital · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInterferon gamma (IFNγ) plays an important role in the development of chronic lung diseases via the production of inflammatory mediators, although the exact mechanism remains unclear. The present study aimed at investigating the potential mechanisms by which IFNγ induced over-production of interleukins through the interaction between carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) and phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) pathway.

methodsIFN-γ induced over-production of interleukin (IL) 6 and IL8, and RNA expression of CEACAM1 and its subtypes or PI3K and its subtypes in human bronchial epithelial cells (HBE). The production of IL6 and IL8 or cell proliferation and movement were also evaluated in cell

resultsCEACAM1, especially CEACAM1-S isoforms, was significantly up-regulated in HBE cells after treatment with IFN-γ. CEACAM1 played roles in expression of IL-6 and IL-8, and facilitated cellular proliferation and migration. IFN-γ up-regulated the expression of CEACAM1 in airway epithelial cells, especially CEACAM1-S isoforms, promoting cellular proliferation, migration, and the production of inflammatory factors. PI3K (p110δ)/Akt/mTOR pathway was involved in the process of IFN-γ-upregulated CEACAM1, especially CEACAM1-S. On the other hand, CEACAM1 could promote the activation of PI3K/Akt/mTOR pathway.

conclusionIFN-γ could induce inflammatory responses, cellular growth and proliferation through the interaction of CEACAM1 (especially CEACAM1-S isoforms) and PI3K(p110δ)/Akt/mTOR in airway epithelial cells, which might be new alternative of future therapies against epithelial transition from inflammation to cancer.

Indexed as

Antigens, CDBronchiCell Adhesion MoleculesCell LineEpithelial CellsHumansInflammationInterferon-gammaModels, BiologicalPhosphatidylinositol 3-KinasesProtein BindingProto-Oncogene Proteins c-aktSignal TransductionAntigens, CDCD66 antigensCell Adhesion MoleculesInterferon-gammaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCEACAM1COPDIFN-γLung cancerPI3K/Akt pathway

Identifiers

PMID31072323
PMCPMC6507156
OpenAlexW2947574275

What OpenQuestion holds

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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.