Evidence map›Paper›PMID 33240904›Full record

ArticleFrontiers in medicine2020

Cigarette Smoke Affects Dendritic Cell Populations, Epithelial Barrier Function, and the Immune Response to Viral Infection With H1N1.

Olga Danov, Martin Wolff, Sabine Bartel, Sebastian Böhlen, Helena Obernolte, Sabine Wronski, Danny Jonigk, Barbara Hammer, Draginja Kovacevic, Sebastian Reuter and 2 more

Abstract read
In one paragraph

Article in Frontiers in medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Review
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  11. Article
  12. Article
  13. Antiviral CD8The European respiratory journal · 2023
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. The lung-gut crosstalk in respiratory and inflammatory bowel disease.Frontiers in cellular and infection microbiology · 2023
    Review
  19. Review
  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

12 authors.

Olga DanovFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Member of Fraunhofer International Consortium for Anti-Infective Research (iCAIR), Member of Centre for Immune Mediated Diseases (CIMD), Hanover, Germany.
Martin WolffEarly Origins of Chronic Lung Diseases, Priority Area Asthma and Allergy, Research Center Borstel - Leibniz Lung Center, Airway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Germany.
Sabine BartelEarly Origins of Chronic Lung Diseases, Priority Area Asthma and Allergy, Research Center Borstel - Leibniz Lung Center, Airway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Germany.
Sebastian BöhlenFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Member of Fraunhofer International Consortium for Anti-Infective Research (iCAIR), Member of Centre for Immune Mediated Diseases (CIMD), Hanover, Germany.
Helena ObernolteFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Member of Fraunhofer International Consortium for Anti-Infective Research (iCAIR), Member of Centre for Immune Mediated Diseases (CIMD), Hanover, Germany.
Sabine WronskiFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Member of Fraunhofer International Consortium for Anti-Infective Research (iCAIR), Member of Centre for Immune Mediated Diseases (CIMD), Hanover, Germany.
Danny JonigkDepartment of Pathology, Hannover Medical School, Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Hanover, Germany.
Barbara HammerEarly Origins of Chronic Lung Diseases, Priority Area Asthma and Allergy, Research Center Borstel - Leibniz Lung Center, Airway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Germany.
Draginja KovacevicEarly Origins of Chronic Lung Diseases, Priority Area Asthma and Allergy, Research Center Borstel - Leibniz Lung Center, Airway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Germany.
Sebastian ReuterEarly Origins of Chronic Lung Diseases, Priority Area Asthma and Allergy, Research Center Borstel - Leibniz Lung Center, Airway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Germany.
Susanne Krauss-EtschmannEarly Origins of Chronic Lung Diseases, Priority Area Asthma and Allergy, Research Center Borstel - Leibniz Lung Center, Airway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Germany.
Katherina SewaldFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Member of Fraunhofer International Consortium for Anti-Infective Research (iCAIR), Member of Centre for Immune Mediated Diseases (CIMD), Hanover, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Smokers with apparently "healthy" lungs suffer from more severe and frequent viral respiratory infections, but the mechanisms underlying this observation are still unclear. Epithelial cells and dendritic cells (DC) form the first line of defense against inhaled noxes such as smoke or viruses. We therefore aimed to obtain insight into how cigarette smoke affects DCs and epithelial cells and how this influences the response to viral infection. Female C57BL/6J mice were exposed to cigarette smoke (CS) for 1 h daily for 24 days and then challenged i.n. with the viral mimic and Toll-like receptor 3 (TLR3) ligand poly (I:C) after the last exposure. DC subpopulations were analyzed 24 h later in whole lung homogenates by flow cytometry. Calu-3 cells or human precision-cut lung slices (PCLS) cultured at air-liquid interface were exposed to CS or air and subsequently inoculated with influenza H1N1. At 48 h post infection cytokines were analyzed by multiplex technology. Cytotoxic effects were measured by release of lactate dehydrogenase (LDH) and confocal imaging. In Calu-3 cells the trans-epithelial electrical resistance (TEER) was assessed. Smoke exposure of mice increased numbers of inflammatory and plasmacytoid DCs in lung tissue. Additional poly (I:C) challenge further increased the population of inflammatory DCs and conventional DCs, especially CD11b

Indexed as

cigarette smoke exposuredendritic cellsepithelial barrierinfluenza virusmouse modelprecision-cut lung slice

Identifiers

PMID33240904
PMCPMC7678748

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Registered trials

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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.