Evidence map›Paper›PMID 37587162›Full record

ArticleInternational journal of obesity (2005)2023

Thoracic adipose tissue contributes to severe virus infection of the lung.

Franziska Hornung, Luise Schulz, Nilay Köse-Vogel, Antje Häder, Jana Grießhammer, Daniel Wittschieber, Angelina Autsch, Christina Ehrhardt, Gita Mall, Bettina Löffler and 1 more

Open access · hybridAbstract read
In one paragraph

Article in International journal of obesity (2005), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 16 citations in OpenAlex.

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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

11 authors at 3 institutions in 1 country.

Franziska HornungInstitute of Medical Microbiology, Jena University Hospital, Am Klinikum 1, Jena, Germany. Franziska.hornung@med.uni-jena.de.ORCID 0000-0002-9942-5572
Luise SchulzInstitute of Medical Microbiology, Jena University Hospital, Am Klinikum 1, Jena, Germany.
Nilay Köse-VogelInstitute of Medical Microbiology, Jena University Hospital, Am Klinikum 1, Jena, Germany.
Antje HäderInstitute of Medical Microbiology, Jena University Hospital, Am Klinikum 1, Jena, Germany.
Jana GrießhammerInstitute of Medical Microbiology, Jena University Hospital, Am Klinikum 1, Jena, Germany.
Daniel WittschieberInstitute of Forensic Medicine, Jena University Hospital, Am Klinikum 1, Jena, Germany.
Angelina AutschInstitute of Forensic Medicine, Jena University Hospital, Am Klinikum 1, Jena, Germany.
Christina EhrhardtSection of Experimental Virology, Institute of Medical Microbiology, Center for Molecular Biomedicine (CMB), Jena University Hospital, Hans-Knoell-Straße 2, Jena, Germany.ORCID 0000-0002-8879-6087
Gita MallInstitute of Forensic Medicine, Jena University Hospital, Am Klinikum 1, Jena, Germany.
Bettina LöfflerInstitute of Medical Microbiology, Jena University Hospital, Am Klinikum 1, Jena, Germany.
Stefanie Deinhardt-EmmerInstitute of Medical Microbiology, Jena University Hospital, Am Klinikum 1, Jena, Germany. Stefanie.deinhardt-emmer@med.uni-jena.de.
Jena University Hospital · DELeibniz Institute of Photonic Technology · DEUniversity Hospital Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveObesity is an independent risk factor for severe influenza virus and COVID-19 infections. There might be an interplay between adipose tissue and respiratory pathogens, although the mechanism is unknown. Proinflammatory factors secreted by the adipose tissue are often discussed to serve as indirect contributor to virus infection. However, the direct potential of adipose tissue to serve as a viral niche has not yet been investigated.

methodsTwo murine obesity models (DIO and ob/ob) were infected with influenza A virus (IAV) and monitored for 3 weeks. p.i. Lung and adipose tissue were harvested, and the viral load was analysed. Direct replication of IAV in vitro was investigated in human derived primary adipocytes and macrophages. The indirect impact of the secretory products of adipocytes during infection was analysed in a co-culture system with lung fibroblasts. Moreover, lung and adipose tissue was harvested from deceased patients infected with SARS-CoV-2 omicron variant. Additionally, replication of SARS-CoV-2 alpha, delta, and omicron variants was investigated in vitro in adipocytes and macrophages.

resultsBoth murine obesity models presented high IAV titers compared to non-obese mice. Interestingly, adipose tissue adjacent to the lungs was a focal point for influenza virus replication in mice. We further detected IAV replication and antiviral response in human adipocytes. Co-cultivation of adipocytes and lung fibroblasts led to increased IL-8 concentration during infection. Though we observed SARS-CoV-2 in the thoracic adipose tissue of COVID-19 patients, no active replication was found in adipocytes in vitro. However, SARS-CoV-2 was detected in the macrophages and this finding was associated with increased inflammation.

conclusionsOur study revealed that thoracic adipose tissue contributes to respiratory virus infection. Besides indirect induction of proinflammatory factors during infection, adipocytes and macrophages within the tissue can directly support viral replication.

Indexed as

COVID-19Influenza A virusInfluenza, HumanAdipose TissueAnimalsHumansLungMiceObesity

Identifiers

PMID37587162
PMCPMC10599992
OpenAlexW4385878433

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.