Evidence map›Paper›PMID 29411515›Full record

ArticleJournal of cellular and molecular medicine2018

SIRT1/FoxO3 axis alteration leads to aberrant immune responses in bronchial epithelial cells.

Serena Di Vincenzo, Irene H Heijink, Jacobien A Noordhoek, Chiara Cipollina, Liboria Siena, Andreina Bruno, Maria Ferraro, Dirkje S Postma, Mark Gjomarkaj, Elisabetta Pace

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Mechanisms and markers of lung ageing in health and disease.European respiratory review : an official journal of the European Respiratory Society · 2025
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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

10 authors at 2 institutions in 2 countries.

Serena Di VincenzoIstituto di Biomedicina e Immunologia Molecolare-Consiglio Nazionale delle Ricerche, Palermo, Italy.
Irene H HeijinkDepartment of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Jacobien A NoordhoekDepartment of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Chiara CipollinaIstituto di Biomedicina e Immunologia Molecolare-Consiglio Nazionale delle Ricerche, Palermo, Italy.
Liboria SienaIstituto di Biomedicina e Immunologia Molecolare-Consiglio Nazionale delle Ricerche, Palermo, Italy.
Andreina BrunoIstituto di Biomedicina e Immunologia Molecolare-Consiglio Nazionale delle Ricerche, Palermo, Italy.
Maria FerraroIstituto di Biomedicina e Immunologia Molecolare-Consiglio Nazionale delle Ricerche, Palermo, Italy.
Dirkje S PostmaDepartment of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Mark GjomarkajIstituto di Biomedicina e Immunologia Molecolare-Consiglio Nazionale delle Ricerche, Palermo, Italy.
Elisabetta PaceIstituto di Biomedicina e Immunologia Molecolare-Consiglio Nazionale delle Ricerche, Palermo, Italy.ORCID 0000-0003-1141-9010
Istituto di Biomedicina e di Immunologia Molecolare Alberto Monroy · ITUniversity Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation and ageing are intertwined in chronic obstructive pulmonary disease (COPD). The histone deacetylase SIRT1 and the related activation of FoxO3 protect from ageing and regulate inflammation. The role of SIRT1/FoxO3 in COPD is largely unknown. This study evaluated whether cigarette smoke, by modulating the SIRT1/FoxO3 axis, affects airway epithelial pro-inflammatory responses. Human bronchial epithelial cells (16HBE) and primary bronchial epithelial cells (PBECs) from COPD patients and controls were treated with/without cigarette smoke extract (CSE), Sirtinol or FoxO3 siRNA. SIRT1, FoxO3 and NF-κB nuclear accumulation, SIRT1 deacetylase activity, IL-8 and CCL20 expression/release and the release of 12 cytokines, neutrophil and lymphocyte chemotaxis were assessed. In PBECs, the constitutive FoxO3 expression was lower in patients with COPD than in controls. Furthermore, CSE reduced FoxO3 expression only in PBECs from controls. In 16HBE, CSE decreased SIRT1 activity and nuclear expression, enhanced NF-κB binding to the IL-8 gene promoter thus increasing IL-8 expression, decreased CCL20 expression, increased the neutrophil chemotaxis and decreased lymphocyte chemotaxis. Similarly, SIRT1 inhibition reduced FoxO3 expression and increased nuclear NF-κB. FoxO3 siRNA treatment increased IL-8 and decreased CCL20 expression in 16HBE. In conclusion, CSE impairs the function of SIRT1/FoxO3 axis in bronchial epithelium, dysregulating NF-κB activity and inducing pro-inflammatory responses.

Indexed as

BronchiChemokine CCL20Cigarette SmokingEpithelial CellsForkhead Box Protein O3Gene Expression RegulationHumansImmunity, CellularInflammationInterleukin-8NF-kappa BNicotianaPulmonary Disease, Chronic ObstructiveRespiratory MucosaSirtuin 1Chemokine CCL20Forkhead Box Protein O3FOXO3 protein, humanInterleukin-8NF-kappa BSIRT1 protein, humanSirtuin 1ageingbronchial epithelial cellscigarette smokeimmune responseinflammationSIRT1/FoxO3

Identifiers

PMID29411515
PMCPMC5867095
OpenAlexW2788303084

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.