Evidence map›Paper›PMID 29813133›Full record

ArticlePLoS pathogens2018

IL-17 can be protective or deleterious in murine pneumococcal pneumonia.

Neil D Ritchie, Ryan Ritchie, Hannah K Bayes, Tim J Mitchell, Tom J Evans

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2018. 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
4.2field-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, 54 citations in OpenAlex.

  1. Article
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  15. Neutrophil Recruitment in Pneumococcal Pneumonia.Frontiers in cellular and infection microbiology · 2022
    Review
  16. Contribution of Puma to Inflammatory Resolution During Early Pneumococcal Pneumonia.Frontiers in cellular and infection microbiology · 2022
    Article
  17. Article
  18. Article
  19. [Research advances on the regulation of interleukin-17 signal transduction and the implication of interleukin-17 in sepsis].Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns · 2021
    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

5 authors at 2 institutions in 1 country.

Neil D RitchieInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.ORCID 0000-0003-3781-2240
Ryan RitchieInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.
Hannah K BayesInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.
Tim J MitchellInstitute of Microbiology and Infection, College of Medical and Dental Sciences University of Birmingham, Birmingham, United Kingdom.ORCID 0000-0002-8309-5556
Tom J EvansInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.ORCID 0000-0002-4140-6352
University of Glasgow · GBUniversity of Birmingham · GB

Funding

Medical Research Council G1001998Wellcome Trust
6 · The paper itself

Abstract

Streptococcus pneumoniae is the major bacterial cause of community-acquired pneumonia, and the leading agent of childhood pneumonia deaths worldwide. Nasal colonization is an essential step prior to infection. The cytokine IL-17 protects against such colonization and vaccines that enhance IL-17 responses to pneumococcal colonization are being developed. The role of IL-17 in host defence against pneumonia is not known. To address this issue, we have utilized a murine model of pneumococcal pneumonia in which the gene for the IL-17 cytokine family receptor, Il17ra, has been inactivated. Using this model, we show that IL-17 produced predominantly from γδ T cells protects mice against death from the invasive TIGR4 strain (serotype 4) which expresses a relatively thin capsule. However, in pneumonia produced by two heavily encapsulated strains with low invasive potential (serotypes 3 and 6B), IL-17 significantly enhanced mortality. Neutrophil uptake and killing of the serotype 3 strain was significantly impaired compared to the serotype 4 strain and depletion of neutrophils with antibody enhanced survival of mice infected with the highly encapsulated SRL1 strain. These data strongly suggest that IL-17 mediated neutrophil recruitment to the lungs clears infection from the invasive TIGR4 strain but that lung neutrophils exacerbate disease caused by the highly encapsulated pneumococcal strains. Thus, whilst augmenting IL-17 immune responses against pneumococci may decrease nasal colonization, this may worsen outcome during pneumonia caused by some strains.

Indexed as

AnimalsBacteremiaBacterial CapsulesBronchoalveolar Lavage FluidDisease Models, AnimalInterleukin-17LungMiceMice, Inbred C57BLMice, KnockoutMicroscopy, Electron, TransmissionMicroscopy, FluorescenceNasopharynxNeutrophilsPeroxidasePhagocytosisIl17ra protein, mouseInterleukin-17PeroxidaseReceptors, Antigen, T-Cell, gamma-deltaReceptors, Interleukin-17

Identifiers

PMID29813133
PMCPMC5993294
OpenAlexW2805129947

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.