Evidence map›Paper›PMID 36396144›Full record

ArticleThe European respiratory journal2023

GPR183 antagonism reduces macrophage infiltration in influenza and SARS-CoV-2 infection.

Cheng Xiang Foo, Stacey Bartlett, Keng Yih Chew, Minh Dao Ngo, Helle Bielefeldt-Ohmann, Buddhika Jayakody Arachchige, Benjamin Matthews, Sarah Reed, Ran Wang, Christian Smith and 12 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The European respiratory journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.1field-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

38 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  4. Article
  5. Palmitic Acid Promotes Antiviral Innate Immunity via ZDHHC20-Mediated CMPK2 Palmitoylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  6. Article
  7. Article
  8. GPR183 contributes to renal macrophage infiltration and fibrosis in kidney injury.American journal of physiology. Renal physiology · 2026
    Article
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  11. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 4 institutions in 2 countries.

Cheng Xiang FooMater Research Institute, Translational Research Institute, The University of Queensland, Brisbane, Australia.ORCID 0000-0002-7539-7116
Stacey BartlettMater Research Institute, Translational Research Institute, The University of Queensland, Brisbane, Australia.
Keng Yih ChewSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, Australia.
Minh Dao NgoMater Research Institute, Translational Research Institute, The University of Queensland, Brisbane, Australia.
Helle Bielefeldt-OhmannSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, Australia.
Buddhika Jayakody ArachchigeCentre for Clinical Research, The University of Queensland, Brisbane, Australia.
Benjamin MatthewsCentre for Clinical Research, The University of Queensland, Brisbane, Australia.
Sarah ReedCentre for Clinical Research, The University of Queensland, Brisbane, Australia.
Ran WangMater Research Institute, Translational Research Institute, The University of Queensland, Brisbane, Australia.
Christian SmithMater Research Institute, Translational Research Institute, The University of Queensland, Brisbane, Australia.ORCID 0000-0002-8096-2052
Matthew J SweetAustralian Infectious Diseases Research Centre, The University of Queensland, Brisbane, Australia.
Lucy BurrDept of Respiratory Medicine, Mater Adult Hospital, Brisbane, Australia.
Kavita BishtMater Research Institute, Translational Research Institute, The University of Queensland, Brisbane, Australia.
Svetlana ShatunovaMater Research Institute, Translational Research Institute, The University of Queensland, Brisbane, Australia.
Jane E SinclairSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, Australia.
Rhys ParrySchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, Australia.
Yuanhao YangMater Research Institute, Translational Research Institute, The University of Queensland, Brisbane, Australia.
Jean-Pierre LévesqueMater Research Institute, Translational Research Institute, The University of Queensland, Brisbane, Australia.
Alexander KhromykhSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, Australia.
Mette Marie RosenkildeDept of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
Kirsty R ShortSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, Australia.
Katharina RonacherMater Research Institute, Translational Research Institute, The University of Queensland, Brisbane, Australia katharina.ronacher@mater.uq.edu.au.ORCID 0000-0002-6371-1462
The University of Queensland · AUTranslational Research Institute · AUMater Adult Hospital · AUUniversity of Copenhagen · DK

Funding

Altered immune-endocrine axis in type 2 diabetes and tuberculosis riskR01AI116039 · NIAID · STELLENBOSCH UNIVERSITY · PI KLEYNHANS, LEANIE, RESTREPO, BLANCA I · 2015 to 2019
$1.7M
NIAID NIH HHS R01 AI116039
6 · The paper itself

Abstract

rationaleSevere viral respiratory infections are often characterised by extensive myeloid cell infiltration and activation and persistent lung tissue injury. However, the immunological mechanisms driving excessive inflammation in the lung remain poorly understood.

objectivesTo identify the mechanisms that drive immune cell recruitment in the lung during viral respiratory infections and identify novel drug targets to reduce inflammation and disease severity.

methodsPreclinical murine models of influenza A virus and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.

resultsOxidised cholesterols and the oxysterol-sensing receptor GPR183 were identified as drivers of monocyte/macrophage infiltration to the lung during influenza A virus (IAV) and SARS-CoV-2 infection. Both IAV and SARS-CoV-2 infection upregulated the enzymes cholesterol 25-hydroxylase (CH25H) and cytochrome P450 family 7 subfamily member B1 (CYP7B1) in the lung, resulting in local production of the oxidised cholesterols 25-hydroxycholesterol (25-OHC) and 7α,25-dihydroxycholesterol (7α,25-OHC). Loss-of-function mutation of Gpr183 or treatment with a GPR183 antagonist reduced macrophage infiltration and inflammatory cytokine production in the lungs of IAV- or SARS-CoV-2-infected mice. The GPR183 antagonist significantly attenuated the severity of SARS-CoV-2 infection and viral loads. Analysis of single-cell RNA-sequencing data on bronchoalveolar lavage samples from healthy controls and COVID-19 patients with moderate and severe disease revealed that

conclusionThis study demonstrates that oxysterols drive inflammation in the lung

Indexed as

COVID-19Influenza, HumanAnimalsCholesterolHumansInflammationLungMacrophagesMiceReceptors, G-Protein-CoupledSARS-CoV-2CholesterolGpr183 protein, mouseReceptors, G-Protein-Coupled

Identifiers

PMID36396144
PMCPMC9686317
OpenAlexW4309366583

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.