Evidence map›Paper›PMID 38109685›Full record

ArticleThe Journal of infectious diseases2024

Severe Acute Respiratory Syndrome Coronavirus 2 Infection Alters Mediators of Lung Tissue Remodeling In Vitro and In Vivo.

Michael Wong, Chandrima Gain, Madhav B Sharma, Leila Fotooh Abadi, Cristelle Hugo, Hariclea Vassilopoulos, Maria Daskou, Gregory A Fishbein, Theodoros Kelesidis

Abstract read
In one paragraph

Article in The Journal of infectious diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Michael WongDivision of Infectious Diseases, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles.
Chandrima GainDivision of Infectious Diseases, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles.
Madhav B SharmaDivision of Infectious Diseases, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles.
Leila Fotooh AbadiDivision of Infectious Diseases, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles.
Cristelle HugoDivision of Infectious Diseases, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles.
Hariclea VassilopoulosDivision of Infectious Diseases, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles.
Maria DaskouDivision of Infectious Diseases, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles.
Gregory A FishbeinDepartment of Pathology, David Geffen School of Medicine, University of California, Los Angeles.
Theodoros KelesidisDivision of Infectious Diseases, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles.ORCID 0000-0002-8463-3811

Funding

Targeting early instigators of vascular inflammation to prevent and/or delay vascular aging in chronic treated HIVR01AG059502 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI KELESIDIS, THEODOROS · 2018 to 2022
$2.0M
NIA NIH HHS R01 AG059502
6 · The paper itself

Abstract

backgroundAltered mediators of airway tissue remodeling such as matrix metalloproteinases (MMPs) in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection may contribute to morbidity in coronavirus disease 2019 (COVID-19); however, the differential impact of SARS-CoV-2 variants of concern (VOCs) on MMPs is unknown.

methodsUsing both in vitro human airway cell culture model and in vivo transgenic mouse model of SARS-CoV-2 infection, we studied the differential effect of SARS-CoV-2 VOCs on expression of key MMPs and inflammatory mediators in airway cells and tissues.

resultsThe most consistent findings with all SARS-CoV-2 variants in infected compared to uninfected human bronchial epithelial cell air-liquid interface cultures were the SARS-CoV-2-induced increases in MMP-12 and tissue inhibitor of MMPs. Infection with both SARS-CoV-2 wild type and SARS-CoV-2 Delta variant over 3 days postinfection (dpi) and with Beta variant over 7 dpi increased lung tissue levels of MMP-9 compared to uninfected mice. Overall, SARS-CoV-2 variants had differential dose-dependent impact on secretion of MMP-1, MMP-2, MMP-9, and MMP-12 that varied at the protein versus the gene level and in the early noninflammatory compared to late inflammatory phase of infection.

conclusionsWe provide novel mechanistic insight that the differential impact of SARS-CoV-2 variants on severity of COVID-19 may partially be attributed to unique changes in MMPs.

Indexed as

COVID-19LungMatrix Metalloproteinase 12Mice, TransgenicSARS-CoV-2Airway RemodelingAnimalsDisease Models, AnimalEpithelial CellsHumansMatrix Metalloproteinase 9Matrix MetalloproteinasesMiceMatrix Metalloproteinase 12Matrix Metalloproteinase 9Matrix Metalloproteinaseslung injurylung tissue remodelingmatrix metalloproteinasesSARS-CoV-2 infectionsevere COVID-19

Identifiers

PMID38109685
PMCPMC13032010

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.