Evidence map›Paper›PMID 35577892›Full record

ArticleScientific reports2022

Anti-nucleocapsid antibodies enhance the production of IL-6 induced by SARS-CoV-2 N protein.

Emi E Nakayama, Ritsuko Kubota-Koketsu, Tadahiro Sasaki, Keita Suzuki, Kazuko Uno, Jun Shimizu, Toru Okamoto, Hisatake Matsumoto, Hiroshi Matsuura, Shoji Hashimoto and 6 more

Abstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
–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

19 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. Antibody-dependent enhancement of coronaviruses.International journal of biological sciences · 2025
    Review
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  12. RAGE Is a Receptor for SARS-CoV-2 N Protein and Mediates N Protein-induced Acute Lung Injury.American journal of respiratory cell and molecular biology · 2023
    Article
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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

16 authors.

Emi E NakayamaResearch Institute for Microbial Diseases and Center for Infectious Disease Education and Research, Osaka University, Suita, Osaka, 565-0871, Japan. emien@biken.osaka-u.ac.jp.
Ritsuko Kubota-KoketsuResearch Institute for Microbial Diseases and Center for Infectious Disease Education and Research, Osaka University, Suita, Osaka, 565-0871, Japan.
Tadahiro SasakiResearch Institute for Microbial Diseases and Center for Infectious Disease Education and Research, Osaka University, Suita, Osaka, 565-0871, Japan.
Keita SuzukiResearch Institute for Microbial Diseases and Center for Infectious Disease Education and Research, Osaka University, Suita, Osaka, 565-0871, Japan.
Kazuko UnoDivision of Basic Research, Louis Pasteur Center for Medical Research, Kyoto, 606-8225, Japan.
Jun ShimizuMiCAN Technologies Inc., Kyoto, 615-8245, Japan.
Toru OkamotoInstitute for Advanced Co-Creation Studies, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, 565-0781, Japan.
Hisatake MatsumotoTrauma and Acute Critical Care Center, Osaka University, Suita, Osaka, 565-0871, Japan.
Hiroshi MatsuuraOsaka Prefectural Nakakawachi Emergency and Critical Care Center, Higashiosaka, Osaka, 678-0947, Japan.
Shoji HashimotoOsaka Prefectural Hospital Organization Osaka Habikino Medical Center, Habikino, Osaka, 583-8588, Japan.
Toshio TanakaOsaka Prefectural Hospital Organization Osaka Habikino Medical Center, Habikino, Osaka, 583-8588, Japan.
Hiromasa HaradaYao Tokushukai General Hospital, Yao, Osaka, 581-0011, Japan.
Masafumi TomitaKobe Tokushukai Hospital, Kobe, Hyogo, 655-0017, Japan.
Mitsunori KanekoSuita Tokushukai Hospital, Suita, Osaka, 565-0814, Japan.
Kazuyuki YoshizakiInstitute of Scientific and Industry Research, Osaka University, Ibaraki, Osaka, 567-0047, Japan.
Tatsuo ShiodaResearch Institute for Microbial Diseases and Center for Infectious Disease Education and Research, Osaka University, Suita, Osaka, 565-0871, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A cytokine storm induces acute respiratory distress syndrome, the main cause of death in coronavirus disease 2019 (COVID-19) patients. However, the detailed mechanisms of cytokine induction due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remain unclear. To examine the cytokine production in COVID-19, we mimicked the disease in SARS-CoV-2-infected alveoli by adding the lysate of SARS-CoV-2-infected cells to cultured macrophages or induced pluripotent stem cell-derived myeloid cells. The cells secreted interleukin (IL)-6 after the addition of SARS-CoV-2-infected cell lysate. Screening of 25 SARS-CoV-2 protein-expressing plasmids revealed that the N protein-coding plasmid alone induced IL-6 production. The addition of anti-N antibody further enhanced IL-6 production, but the F(ab')

Indexed as

Antibodies, ViralCoronavirus Nucleocapsid ProteinsCOVID-19Interleukin-6SARS-CoV-2Cytokine Release SyndromeCytokinesHumansPhosphoproteinsAntibodies, ViralCoronavirus Nucleocapsid ProteinsCytokinesInterleukin-6nucleocapsid phosphoprotein, SARS-CoV-2Phosphoproteins

Identifiers

PMID35577892
PMCPMC9109953

What OpenQuestion holds

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LicenceCC BY
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.