Evidence map›Paper›PMID 33411748›Full record

ArticlePloS one2021

IL-17C contributes to NTHi-induced inflammation and lung damage in experimental COPD and is present in sputum during acute exacerbations.

Giovanna Vella, Felix Ritzmann, Lisa Wolf, Andreas Kamyschnikov, Hannah Stodden, Christian Herr, Hortense Slevogt, Robert Bals, Christoph Beisswenger

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.7field-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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. The role of IL-17 family cytokines in cardiac fibrosis.Frontiers in cardiovascular medicine · 2024
    Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Blockade of PD-1 decreases neutrophilic inflammation and lung damage in experimental COPD.American journal of physiology. Lung cellular and molecular physiology · 2021
    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

9 authors at 2 institutions in 1 country.

Giovanna VellaDepartment of Internal Medicine V - Pulmonology, Allergology and Respiratory Critical Care Medicine, Saarland University, Homburg, Germany.
Felix RitzmannDepartment of Internal Medicine V - Pulmonology, Allergology and Respiratory Critical Care Medicine, Saarland University, Homburg, Germany.
Lisa WolfDepartment of Internal Medicine V - Pulmonology, Allergology and Respiratory Critical Care Medicine, Saarland University, Homburg, Germany.
Andreas KamyschnikovDepartment of Internal Medicine V - Pulmonology, Allergology and Respiratory Critical Care Medicine, Saarland University, Homburg, Germany.
Hannah StoddenDepartment of Internal Medicine V - Pulmonology, Allergology and Respiratory Critical Care Medicine, Saarland University, Homburg, Germany.
Christian HerrDepartment of Internal Medicine V - Pulmonology, Allergology and Respiratory Critical Care Medicine, Saarland University, Homburg, Germany.
Hortense SlevogtSeptomics Research Center, Jena University Hospital, Jena, Germany.
Robert BalsDepartment of Internal Medicine V - Pulmonology, Allergology and Respiratory Critical Care Medicine, Saarland University, Homburg, Germany.
Christoph BeisswengerDepartment of Internal Medicine V - Pulmonology, Allergology and Respiratory Critical Care Medicine, Saarland University, Homburg, Germany.ORCID 0000-0003-4391-3240
Saarland University · DEJena University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophilic inflammation results in loss of lung function in chronic obstructive pulmonary disease (COPD). Gram-negative bacteria, such as nontypeable Haemophilus influenzae (NTHi), trigger acute exacerbations of COPD (AECOPD) and contribute to chronic lung inflammation. The pro-inflammatory cytokine interleukin-17C (IL-17C) is expressed by airway epithelial cells and regulates neutrophilic chemotaxis. Here, we explored the function of IL-17C in NTHi- and cigarette smoke (CS)-induced models of COPD. Neutrophilic inflammation and tissue destruction were decreased in lungs of IL-17C-deficient mice (Il-17c-/-) chronically exposed to NTHi. Numbers of pulmonary neutrophils were decreased in Il-17c-/- mice after acute exposure to the combination of NTHi and CS. However, Il-17c-/- mice were not protected from CS-induced lung inflammation. In a preliminary patient study, we show that IL-17C is present in sputum samples obtained during AECOPD and associates with disease severity. Concentrations of IL-17C were significantly increased during advanced COPD (GOLD III/IV) compared to moderate COPD (GOLD I/II). Concentrations of IL-17A and IL-17E did not associate with disease severity. Our data suggest that IL-17C promotes harmful pulmonary inflammation triggered by bacteria in COPD.

Indexed as

Disease ProgressionAcute DiseaseAgedAnimalsCigarette SmokingCytokinesFemaleHaemophilus influenzaeHumansInterleukin-17LungMaleMiceMice, Inbred C57BLNeutrophilsPneumoniaCytokinesInterleukin-17

Identifiers

PMID33411748
PMCPMC7790230
OpenAlexW3120027527

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.