Evidence map›Paper›PMID 23490254›Full record

ArticleThe American journal of pathology2013

IL-22 is essential for lung epithelial repair following influenza infection.

Derek A Pociask, Erich V Scheller, Sivanarayana Mandalapu, Kevin J McHugh, Richard I Enelow, Cheryl L Fattman, Jay K Kolls, John F Alcorn

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed, 1 pooled it
9.8field-weighted citation impact, top 1% 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

145 citing papers in PubMed, 1 synthesis or guideline pooled it, 212 citations in OpenAlex.

  1. Pooled it
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  12. Article
  13. Article
  14. International journal of molecular sciences · 2025
    Article
  15. Review
  16. I don't know about you, but I'm feeling IL-22.Cytokine & growth factor reviews · 2024
    Review
  17. Article
  18. Sex-based differences in persistent lung inflammation following influenza infection of juvenile outbred mice.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  19. Article
  20. Article

85 more citing papers are in PubMed but not listed here.

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

8 authors at 4 institutions in 1 country.

Derek A PociaskRichard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA.
Erich V Scheller
Sivanarayana Mandalapu
Kevin J McHugh
Richard I Enelow
Cheryl L Fattman
Jay K Kolls
John F Alcorn
Children's Hospital of Pittsburgh · USUniversity of Pittsburgh Medical Center · USDartmouth Psychiatric Research Center · USUniversity of Pittsburgh · US

Funding

University of Pittsburgh Clinical and Translational Science InstituteUL1TR000005 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$50.8M
Influenza A Inhibits TH17 Host Defense Against Bacterial PneumoniaR01HL107380 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ALCORN, JOHN F · 2012 to 2024
$5.4M
Th17 Cytokines and Lung ImmunityR37HL079142 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KOLLS, JAY K · 2010 to 2017
$3.6M
IL-23 / Il-17 and Lung Host DefenseR01HL079142 · NHLBI · LSU HEALTH SCIENCES CENTER · PI KOLLS, JAY K · 2005 to 2009
$1.9M
NCATS NIH HHS UL1 TR000005NHLBI NIH HHS HL079142NHLBI NIH HHS HL107380NHLBI NIH HHS R01 HL079142NHLBI NIH HHS R01 HL107380NHLBI NIH HHS R37 HL079142
6 · The paper itself

Abstract

Influenza infection is widespread in the United States and the world. Despite low mortality rates due to infection, morbidity is common and little is known about the molecular events involved in recovery. Influenza infection results in persistent distal lung remodeling, and the mechanism(s) involved are poorly understood. Recently IL-22 has been found to mediate epithelial repair. We propose that IL-22 is critical for recovery of normal lung function and architecture after influenza infection. Wild-type and IL-22(-/-) mice were infected with influenza A PR8/34 H1N1 and were followed up for up to 21 days post infection. IL-22 receptor was localized to the airway epithelium in naive mice but was expressed at the sites of parenchymal lung remodeling induced by influenza infection. IL-22(-/-) mice displayed exacerbated lung injury compared with wild-type mice, which correlated with decreased lung function 21 days post infection. Epithelial metaplasia was observed in wild-type mice but was not evident in IL-22(-/-) animals that were characterized with an increased fibrotic phenotype. Gene expression analysis revealed aberrant expression of epithelial genes involved in repair processes, among changes in several other biological processes. These data indicate that IL-22 is required for normal lung repair after influenza infection. IL-22 represents a novel pathway involved in interstitial lung disease.

Indexed as

Wound HealingAnimalsBasement MembraneCollagenEpithelial CellsEpitheliumGene Expression ProfilingGene Expression RegulationInterleukin-22InterleukinsLungMetaplasiaMiceMice, Inbred C57BLOrthomyxoviridae InfectionsReceptors, InterleukinCollagenInterleukin-22interleukin-22 receptorInterleukinsReceptors, Interleukin

Identifiers

PMID23490254
PMCPMC3620404
OpenAlexW2163381313

What OpenQuestion holds

Textmetadata
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.