Evidence map›Paper›PMID 27375092›Full record

ArticleJournal of cystic fibrosis : official journal of the European Cystic Fibrosis Society2016

IL-22 exacerbates weight loss in a murine model of chronic pulmonary Pseudomonas aeruginosa infection.

Hannah K Bayes, Neil D Ritchie, Christopher Ward, Paul A Corris, Malcolm Brodlie, Thomas J Evans

Open access · hybridAbstract read
In one paragraph

Article in Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. The Role of Group 3 Innate Lymphoid Cells in Lung Infection and Immunity.Frontiers in cellular and infection microbiology · 2021
    Review
  4. Article
  5. Review of PotentialJournal of fungi (Basel, Switzerland) · 2020
    Review
  6. Review
  7. Article
  8. Article
  9. 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

6 authors at 2 institutions in 1 country.

Hannah K BayesInstitute of Infection, Immunity and Inflammation, University of Glasgow, G12 8TA, United Kingdom. Electronic address: hannah.bayes@talk21.com.
Neil D RitchieInstitute of Cellular Medicine, Newcastle University, Framlington Place, Newcastle upon Tyne NE2 4HH, UK.
Christopher WardInstitute of Cellular Medicine, Newcastle University, Framlington Place, Newcastle upon Tyne NE2 4HH, UK.
Paul A CorrisInstitute of Cellular Medicine, Newcastle University, Framlington Place, Newcastle upon Tyne NE2 4HH, UK; Institute of Transplantation, Freeman Hospital, Newcastle upon Tyne NE7 7DN, UK.
Malcolm BrodlieInstitute of Cellular Medicine, Newcastle University, Framlington Place, Newcastle upon Tyne NE2 4HH, UK; Paediatric Respiratory Medicine, Great North Children's Hospital, Queen Victoria Road, Newcastle upon Tyne NE1 4LP, UK.
Thomas J EvansInstitute of Infection, Immunity and Inflammation, University of Glasgow, G12 8TA, United Kingdom.
Newcastle University · GBUniversity of Glasgow · GB

Funding

Medical Research Council G0800419Medical Research Council MR/M008797/1Wellcome TrustWellcome Trust 094779
6 · The paper itself

Abstract

backgroundInterleukin (IL)-22 is a critical mediator of mucosal immunity and tissue regeneration, protecting against a number of respiratory pathogens. Whether IL-22 confers protection against chronic Pseudomonas aeruginosa (PA) infection in cystic fibrosis (CF) is unknown.

methodsExplanted CF lungs were examined for IL-22 production and immune-localization. A murine model of persistent pulmonary PA infection was used to examine production of IL-22 following infective challenge. The role of IL-22 was examined using IL-22 knockout (KO) animals.

resultsIL-22 is produced within the adult CF lung and localizes to the airway epithelium. IL-22 is produced by murine pulmonary lymph node cells following lung infection. The absence of IL-22 resulted in no significant difference in acute mortality, bacterial burden, chronic infection rates, histological changes or neutrophilic inflammation in the chronic PA infection model. However, IL-22 KO animals lost less weight following infection.

conclusionIL-22 is produced in the CF lung and in response to PA infection yet is dispensable in protection against chronic pulmonary P. aeruginosa infection in a murine model. However, we identified a novel role for the cytokine in promoting infection-related weight-loss, a significant prognostic factor in the CF population.

Indexed as

Cystic FibrosisInterleukinsPneumoniaPseudomonas InfectionsAnimalsChronic DiseaseDisease Models, AnimalInterleukin-22LungMiceMucusProtective FactorsPseudomonas aeruginosaInterleukin-22InterleukinsChronic infectionCystic fibrosisInterleukin-22Mucosal immunityPseudomonas aeruginosa

Identifiers

PMID27375092
PMCPMC5154339
OpenAlexW2471359302

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.