Evidence map›Paper›PMID 27456484›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Critical Role of IL-22/IL22-RA1 Signaling in Pneumococcal Pneumonia.

Giraldina Trevejo-Nunez, Waleed Elsegeiny, Parker Conboy, Kong Chen, Jay K Kolls

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 51 citations in OpenAlex.

  1. Trial
  2. Article
  3. Animals : an open access journal from MDPI · 2025
    Article
  4. I don't know about you, but I'm feeling IL-22.Cytokine & growth factor reviews · 2024
    Review
  5. Article
  6. IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. The Role of Group 3 Innate Lymphoid Cells in Lung Infection and Immunity.Frontiers in cellular and infection microbiology · 2021
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  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 1 institution in 1 country.

Giraldina Trevejo-NunezRichard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh of UPMC, University of Pittsburgh, Pittsburgh, PA 15224.
Waleed ElsegeinyRichard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh of UPMC, University of Pittsburgh, Pittsburgh, PA 15224.
Parker ConboyRichard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh of UPMC, University of Pittsburgh, Pittsburgh, PA 15224.
Kong ChenRichard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh of UPMC, University of Pittsburgh, Pittsburgh, PA 15224.ORCID 0000-0001-6980-5454
Jay K KollsRichard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh of UPMC, University of Pittsburgh, Pittsburgh, PA 15224 jay.kolls@chp.edu.
University of Pittsburgh · US

Funding

Translational StudiesP30DK072506 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PILEWSKI, JOSEPH MARK · 2005 to 2017
$12.5M
Th17 Cytokines and Lung ImmunityR37HL079142 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KOLLS, JAY K · 2010 to 2017
$3.6M
NHLBI NIH HHS R37 HL079142NIDDK NIH HHS P30 DK072506
6 · The paper itself

Abstract

IL-22-IL-22R signaling plays a crucial role in regulating host defenses against extracellular pathogens, particularly in the intestine, through the induction of antimicrobial peptides and chemotactic genes. However, the role of IL-22-IL-22R is understudied in Streptococcus pneumoniae lung infection, a prevalent pathogen of pneumonia. This paper presents the findings of IL-22 signaling during a murine model of pneumococcal pneumonia and improvement of bacterial burden upon IL-22 administration. IL-22 was rapidly induced in the lung during pneumococcal infection in wild-type mice, and Il22(-/-) mice had higher pneumococcal burdens compared with controls. Additionally, mice with hepatic-specific deletion of Il22ra1 also had higher bacterial burdens in lungs compared with littermate controls after intrapulmonary pneumococcal infection, suggesting that IL-22 signaling in the liver is important to control pneumococcal pneumonia. Thus, we hypothesized that enhancement of IL-22 signaling would control pneumococcal burden in lung tissues in an experimental pneumonia model. Administration of rIL-22 systemically to infected wild-type mice decreased bacterial burden in lung and liver at 24 h postinfection. Our in vitro studies also showed that mice treated with IL-22 had increased C3 expression in the liver compared with the isotype control group. Furthermore, serum from mice treated with IL-22 had improved opsonic capacity by increasing C3 binding on S. pneumoniae Taken together, endogenous IL-22 and hepatic IL-22R signaling play critical roles in controlling pneumococcal lung burden, and systemic IL-22 decreases bacterial burden in the lungs and peripheral organs by potentiating C3 opsonization on bacterial surfaces, through the increase of hepatic C3 expression.

Indexed as

Signal TransductionAnimalsBacterial LoadComplement C3CytokinesInterleukin-22InterleukinsLiverLungMiceMice, Inbred C57BLPhagocytosisPneumonia, PneumococcalReceptors, InterleukinStreptococcus pneumoniaeComplement C3CytokinesInterleukin-22interleukin-22 receptorInterleukinsReceptors, Interleukin

Identifiers

PMID27456484
PMCPMC4992592
OpenAlexW2480280064

What OpenQuestion holds

Textmetadata
LicenceTDM
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.