Evidence map›Paper›PMID 28260794›Full record

ArticleCellular & molecular immunology2018

Aberrant Th2 inflammation drives dysfunction of alveolar macrophages and susceptibility to bacterial pneumonia.

Emily K Moser, Natania S Field, Paula M Oliver

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. The ubiquitin ligase Cul5 regulates CD4Nature communications · 2022
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. 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

3 authors at 2 institutions in 1 country.

Emily K MoserCell Pathology Division, Children's Hospital of Philadelphia, 19104, Philadelphia, PA, USA. Emily.k.moser@gmail.com.
Natania S FieldCell and Molecular Biology Program, Perelman School of Medicine, University of Pennsylvania, 19104, Philadelphia, PA, USA.
Paula M OliverCell Pathology Division, Children's Hospital of Philadelphia, 19104, Philadelphia, PA, USA.
University of Pennsylvania · USChildren's Hospital of Philadelphia · US

Funding

TRAINING IN HIV PATHOGENESIST32AI007632 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI Frederic D Bushman, James L. Riley · 2000 to 2026
$10.6M
Nedd4-family adaptors and their regulation of T cell function.R01AI093566 · NIAID · CHILDREN'S HOSP OF PHILADELPHIA · PI OLIVER, PAULA MARIA · 2011 to 2020
$4.2M
Mechanisms of ubiquitin pathway activation and functionR01AI114515 · NIAID · CHILDREN'S HOSP OF PHILADELPHIA · PI OLIVER, PAULA MARIA · 2015 to 2019
$2.1M
NIAID NIH HHS R01 AI093566NIAID NIH HHS R01 AI114515NIAID NIH HHS T32 AI007632
6 · The paper itself

Abstract

The ubiquitin ligase, Itch, is required to prevent autoinflammatory disease in mice and humans. Itch-deficient mice develop lethal pulmonary inflammation characterized by the production of Th2 cytokines (for example, interleukin-4 (IL-4)); however, the contribution of Itch to immune defense against respiratory pathogens has not been determined. We found that Itch-deficient mice were highly susceptible to intranasal infection with the respiratory pathogen Klebsiella pneumoniae. Infected Itch-deficient mice exhibited increased immune cell infiltration, cytokine levels and bacterial burden in the respiratory tract compared with control mice. However, numbers of resident alveolar macrophages were reduced in the lungs from Itch-deficient mice both before and after infection. High levels of Th2 cytokines in the respiratory tract correlated with deceased alveolar macrophages, and genetic ablation of IL-4 restored alveolar macrophages and host defense to K. pneumoniae in Itch-deficient mice, suggesting that loss of alveolar macrophages occurred as a consequence of Th2 inflammation. Adoptive transfer of Itch

Indexed as

Disease SusceptibilityAnimalsCell CountCytokinesInflammationLungMacrophages, AlveolarMicePneumonia, BacterialSignal TransductionSTAT6 Transcription FactorTh2 CellsUbiquitin-Protein LigasesCytokinesItch protein, mouseStat6 protein, mouseSTAT6 Transcription FactorUbiquitin-Protein Ligasesalveolar macrophagebacterial pneumoniaItchTh2 cell

Identifiers

PMID28260794
PMCPMC6068136
OpenAlexW2593775889

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.