Evidence map›Paper›PMID 24918427›Full record

ArticlePloS one2014

Targeting IL-1β and IL-17A driven inflammation during influenza-induced exacerbations of chronic lung inflammation.

Anke Sichelstiel, Koshika Yadava, Aurélien Trompette, Olawale Salami, Yoichiro Iwakura, Laurent P Nicod, Benjamin J Marsland

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.2field-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

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
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  8. Article
  9. The role of Th17 cells: explanation of relationship between periodontitis and COPD?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Review
  10. Article
  11. The protective effect of rheumatic disease agents in COVID-19.Best practice & research. Clinical rheumatology · 2021
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Influenza in High-Risk Hosts-Lessons Learned from Animal Models.Cold Spring Harbor perspectives in medicine · 2020
    Review
  17. Article
  18. Article
  19. Review
  20. Review
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

7 authors at 2 institutions in 2 countries.

Anke SichelstielFaculty of Biology and Medicine, University of Lausanne, Service de Pneumologie, CHUV, Lausanne, Switzerland; Molecular Biomedicine, ETHZ, Zurich, Switzerland.
Koshika YadavaFaculty of Biology and Medicine, University of Lausanne, Service de Pneumologie, CHUV, Lausanne, Switzerland.
Aurélien TrompetteFaculty of Biology and Medicine, University of Lausanne, Service de Pneumologie, CHUV, Lausanne, Switzerland.
Olawale SalamiFaculty of Biology and Medicine, University of Lausanne, Service de Pneumologie, CHUV, Lausanne, Switzerland.
Yoichiro IwakuraResearch Institute for Biomedical Sciences, Tokyo University of Science, Tokyo, Japan.
Laurent P NicodFaculty of Biology and Medicine, University of Lausanne, Service de Pneumologie, CHUV, Lausanne, Switzerland.
Benjamin J MarslandFaculty of Biology and Medicine, University of Lausanne, Service de Pneumologie, CHUV, Lausanne, Switzerland.
University of Lausanne · CHTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

For patients with chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), exacerbations are life-threatening events causing acute respiratory distress that can even lead to hospitalization and death. Although a great deal of effort has been put into research of exacerbations and potential treatment options, the exact underlying mechanisms are yet to be deciphered and no therapy that effectively targets the excessive inflammation is available. In this study, we report that interleukin-1β (IL-1β) and interleukin-17A (IL-17A) are key mediators of neutrophilic inflammation in influenza-induced exacerbations of chronic lung inflammation. Using a mouse model of disease, our data shows a role for IL-1β in mediating lung dysfunction, and in driving neutrophilic inflammation during the whole phase of viral infection. We further report a role for IL-17A as a mediator of IL-1β induced neutrophilia at early time points during influenza-induced exacerbations. Blocking of IL-17A or IL-1 resulted in a significant abrogation of neutrophil recruitment to the airways in the initial phase of infection or at the peak of viral replication, respectively. Therefore, IL-17A and IL-1β are potential targets for therapeutic treatment of viral exacerbations of chronic lung inflammation.

Indexed as

Neutrophil InfiltrationAnimalsAntibodies, NeutralizingChronic DiseaseHumansInfluenza, HumanInterleukin-17Interleukin-1betaInterleukin 1 Receptor Antagonist ProteinMiceMice, Inbred BALB CMice, Inbred C57BLOrthomyxoviridae InfectionsPneumoniaPulmonary Disease, Chronic ObstructiveRecombinant ProteinsAntibodies, NeutralizingInterleukin-17Interleukin-1betaInterleukin 1 Receptor Antagonist ProteinRecombinant Proteins

Identifiers

PMID24918427
PMCPMC4053370
OpenAlexW2026660388

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.