Evidence map›Paper›PMID 39349051›Full record

ArticleLupus science & medicine2024

SARS-CoV-2 spike aggravates lupus nephritis and lung fibrosis in systemic lupus erythematosus.

Yeon Su Lee, Jin Seok Woo, JooYeon Jhun, Jeong Won Choi, A Ram Lee, Kun Hee Lee, Haeyoun Choi, Sung-Hwan Park, Mi-La Cho

Abstract read
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In one paragraph

Article in Lupus science & medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
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.

Yeon Su LeeLab of Translational ImmunoMedicine (LaTIM), Catholic Research Institute of Medical Science, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Jin Seok WooLab of Translational ImmunoMedicine (LaTIM), Catholic Research Institute of Medical Science, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
JooYeon JhunLab of Translational ImmunoMedicine (LaTIM), Catholic Research Institute of Medical Science, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Jeong Won ChoiLab of Translational ImmunoMedicine (LaTIM), Catholic Research Institute of Medical Science, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
A Ram LeeLab of Translational ImmunoMedicine (LaTIM), Catholic Research Institute of Medical Science, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Kun Hee LeeLab of Translational ImmunoMedicine (LaTIM), Catholic Research Institute of Medical Science, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Haeyoun ChoiDepartment of Microbiology, The Catholic University of Korea, Seoul, South Korea.
Sung-Hwan ParkDivision of Rheumatology, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Mi-La ChoLab of Translational ImmunoMedicine (LaTIM), Catholic Research Institute of Medical Science, College of Medicine, The Catholic University of Korea, Seoul, South Korea iammila@catholic.ac.kr.ORCID 0000-0001-5715-3989

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveCOVID-19 induces the development of autoimmune diseases, including SLE, which are characterised by inflammation, autoantibodies and thrombosis. However, the effects of COVID-19 on SLE remain unclear.

methodsWe investigated the effects of COVID-19 on SLE development and progression in three animal models. Plasmids encoding SARS-CoV-2 spike protein and ACE2 receptor were injected into R848-induced BALB/C lupus mice, R848-induced IL-1 receptor antagonist knockout (KO) lupus mice and MRL/lpr mice. Serum levels of albumin and autoantibodies, lymphocyte phenotypes and tissue histology were evaluated.

resultsIn R848-induced BALB/C lupus mice, the SARS-CoV-2 spike protein increased autoantibody and albumin levels compared with vehicle and mock treatments. These mice also exhibited splenomegaly, which was further exacerbated by the spike protein. Flow cytometric analysis revealed elevated T helper 1 cell counts, and histological analysis indicated increased levels of the fibrosis marker protein α-smooth muscle actin. In KO mice, the spike protein induced splenomegaly, severe kidney damage and pronounced lung fibrosis. In the MRL/lpr group, spike protein increased the serum levels of autoantibodies, albumin and the thrombosis marker chemokine (C-X-C motif) ligand 4.

conclusionCOVID-19 accelerated the development and progression of lupus by inducing autoantibody production, fibrosis and thrombosis.

Indexed as

AutoantibodiesCOVID-19Disease Models, AnimalLupus Erythematosus, SystemicLupus NephritisMice, Inbred BALB CMice, KnockoutSARS-CoV-2Spike Glycoprotein, CoronavirusAngiotensin-Converting Enzyme 2AnimalsFemaleMiceMice, Inbred MRL lprPulmonary FibrosisSplenomegalyAngiotensin-Converting Enzyme 2AutoantibodiesSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2COVID-19lupus erythematosus, systemiclupus nephritispulmonary fibrosis

Identifiers

PMID39349051
PMCPMC11448135

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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.