Evidence map›Paper›PMID 36550471›Full record

ArticlePediatric rheumatology online journal2022

Beneficial effects of anti-apolipoprotein A-2 on an animal model for coronary arteritis in Kawasaki disease.

Fuyu Ito, Toshiaki Oharaseki, Daisuke Tsukui, Yoshitaka Kimura, Tamiko Yanagida, Fukuko Kishi, Yoshio Yamakawa, Yosuke Kameoka, Shoichi Suzuki, Kazuko Uno and 6 more

Open access · goldAbstract read
In one paragraph

Article in Pediatric rheumatology online journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. Article
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 at 5 institutions in 1 country.

Fuyu ItoAsia International Institute of Infectious Disease Control and General Medical Education and Research Center, Teikyo University, Kaga 2-11-1, Itabashi-ku, Tokyo, 173-8605, Japan. fufuyou@med.teikyo-u.ac.jp.ORCID http://orcid.org/0000-0003-4295-2926
Toshiaki OharasekiDepartment of Pathology, Toho University Ohashi Medical Center, Ohashi 2-17-6, Meguro-ku, Tokyo, 153-8515, Japan.
Daisuke TsukuiDepartment of Internal Medicine, Teikyo University School of Medicine, Kaga 2-11-1, Itabashi-ku, Tokyo, 173-8605, Japan.
Yoshitaka KimuraDepartment of Internal Medicine, Teikyo University School of Medicine, Kaga 2-11-1, Itabashi-ku, Tokyo, 173-8605, Japan.
Tamiko YanagidaDepartment of Internal Medicine, Teikyo University School of Medicine, Kaga 2-11-1, Itabashi-ku, Tokyo, 173-8605, Japan.
Fukuko KishiDepartment of Research and Development, A-CLIP Institute, Inohana 1-8-15, Chuo-ku, Chiba City, Chiba, 260-0856, Japan.
Yoshio YamakawaDepartment of Research and Development, A-CLIP Institute, Inohana 1-8-15, Chuo-ku, Chiba City, Chiba, 260-0856, Japan.
Yosuke KameokaDepartment of Research and Development, A-CLIP Institute, Inohana 1-8-15, Chuo-ku, Chiba City, Chiba, 260-0856, Japan.
Shoichi SuzukiAsia International Institute of Infectious Disease Control and General Medical Education and Research Center, Teikyo University, Kaga 2-11-1, Itabashi-ku, Tokyo, 173-8605, Japan.
Kazuko UnoLouis Pasteur Center for Medical Research, Tanaka Monzencho 103-5, Sakyo-ku, Kyoto, 606-8225, Japan.
Osamu SuzukiLaboratory of Animal Models for Human Diseases, National Institutes of Biomedical Innovation, Health and Nutrition, Saito-Asagi 7-6-8, Ibaraki City, Osaka, 567-0085, Japan.
Noriko N MiuraLaboratory for Immunology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science, Horinouchi 1432-1, Hachioji, Tokyo, 192-0392, Japan.
Naohito OhnoLaboratory for Immunology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science, Horinouchi 1432-1, Hachioji, Tokyo, 192-0392, Japan.
Kei TakahashiDepartment of Pathology, Toho University Ohashi Medical Center, Ohashi 2-17-6, Meguro-ku, Tokyo, 153-8515, Japan.
Hajime KonoDepartment of Internal Medicine, Teikyo University School of Medicine, Kaga 2-11-1, Itabashi-ku, Tokyo, 173-8605, Japan.
Kazuo SuzukiAsia International Institute of Infectious Disease Control and General Medical Education and Research Center, Teikyo University, Kaga 2-11-1, Itabashi-ku, Tokyo, 173-8605, Japan.
Teikyo University · JPToho University · JPTokyo University of Pharmacy and Life Sciences · JPLouis Pasteur Center for Medical Research · JPNational Institute of Biomedical Innovation, Health and Nutrition · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKawasaki disease (KD) is usually treated with high-dose intravenous immunoglobulin (IVIg) as severe infectious and other diseases. Due to issues that are associated with immunoglobulin preparation, such as the risk of possible contamination by infectious agents and limited blood banking resources, recombinant immunoglobulins are required. We developed a novel recombinant antibody drug candidate, "VasSF," based on the therapeutic effects it exerted on a mouse spontaneous crescentic glomerulonephritis model (SCG/Kj). Apolipoprotein A-2 (ApoA2) has been identified as one of VasSF's target molecules.

methodsHere, we tested the potential of anti-apolipoprotein A-2 antibodies (anti-ApoA2) as a new therapeutic drug against KD by examining its effect on a mouse model, in which KD was induced via Candida albicans water-soluble fraction (CAWS). CAWS (2 mg/mouse) was injected intraperitoneally into C57BL/6NCrSlc mice for five consecutive days. The incidence and histological severity of vasculitis in CAWS-induced coronary arteritis in mice administered anti-ApoA2 was examined. The following experimental groups were tested: solvent (only PBS (-) injection); anti-ApoA2 antibodies at dosages of 0.05 mg, 0.1 mg, and 0.5 mg/kg/day; human IgG at 0.1 mg/kg/day.

resultsThe group treated with anti-ApoA2 0.5 mg/kg/day showed a lower incidence of panvasculitis induced by CAWS, less inflammation of the coronary arteries and aortic roots, and lower levels of serum IL-6, M-CSF, and MIP-1α and 32 cytokines/chemokines compared with those in the solvent group.

conclusionsThe anti-ApoA2 treatment suppressed the development of coronary arteritis in an animal KD model and anti-ApoA2 shows potential as an effective therapeutic candidate for the treatment of KD vasculitis. The use of specific antibodies that display higher vasculitis-suppressing effects, such as anti-ApoA2, may attenuate KD as well as other infectious diseases, with less severe adverse side effects than treatment with IVIg.

Indexed as

ArteritisCoronary Artery DiseaseMucocutaneous Lymph Node SyndromeVasculitisAnimalsCoronary VesselsDisease Models, AnimalHumansImmunoglobulins, IntravenousMiceMice, Inbred C57BLSolventsImmunoglobulins, IntravenousSolventsAnti-apolipoprotein A-2Coronary arteritisKawasaki diseaseVasculitis

Identifiers

PMID36550471
PMCPMC9773535
OpenAlexW4312098544

What OpenQuestion holds

Textmetadata
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.