Evidence map›Paper›PMID 33005412›Full record

ArticleClinical & translational immunology2020

CD163 deficiency facilitates lipopolysaccharide-induced inflammatory responses and endotoxin shock in mice.

Yukio Fujiwara, Koji Ohnishi, Hasita Horlad, Yoichi Saito, Daisuke Shiraishi, Hiroto Takeya, Daiki Yoshii, Shinjiro Kaieda, Tomoaki Hoshino, Yoshihiro Komohara

Open access · goldAbstract read
In one paragraph

Article in Clinical & translational immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Rodent monocyte-derived macrophages do not express CD163: Comparative analysis using macrophages from living boreoeutherians.Developmental dynamics : an official publication of the American Association of Anatomists · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. [Antibacterial mechanism of Brevinin-2GHk, an antimicrobial peptide fromNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
  10. A case of suprasellar Erdheim-Chester disease and characterization of macrophage phenotype.Journal of clinical and experimental hematopathology : JCEH · 2020
    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

10 authors at 2 institutions in 1 country.

Yukio FujiwaraDepartment of Cell Pathology Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Koji OhnishiDepartment of Cell Pathology Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Hasita HorladDepartment of Cell Pathology Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Yoichi SaitoDepartment of Cell Pathology Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Daisuke ShiraishiDepartment of Cell Pathology Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Hiroto TakeyaDepartment of Cell Pathology Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Daiki YoshiiDepartment of Cell Pathology Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Shinjiro KaiedaDivision of Respirology, Neurology, and Rheumatology Department of Medicine Kurume University School of Medicine Kurume Japan.
Tomoaki HoshinoDivision of Respirology, Neurology, and Rheumatology Department of Medicine Kurume University School of Medicine Kurume Japan.
Yoshihiro KomoharaDepartment of Cell Pathology Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Kumamoto University · JPKurume University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesSeptic (or endotoxin) shock is a severe systemic inflammatory disease caused by bacteraemia or endotoxaemia. Although it is known that increased serum levels of CD163 are observed in septic/endotoxin shock patients, the exact function and significance of CD163 in macrophage activation remain unclear. Therefore, in the current study, we tested whether CD163 contributes to the pathogenesis of endotoxin shock in mice. METHODS AND

resultsIn samples obtained from autopsy, the number of CD163-positive macrophages was increased in the kidney, liver, heart, bone marrow and spleen of patients who had died from septic/endotoxin shock when compared to patients who had died from other causes. The animal study revealed a significantly lower survival rate in CD163-deficient mice after lipopolysaccharide (LPS) injection. Several cytokines and oxidative stress-related molecules were significantly elevated in the sera of LPS-induced endotoxin shock mice models. Higher concentrations of IL-6, TNF-α, IL-1β, nitrite (

conclusionsCD163 was suggested to be involved in the regulation of inflammatory cytokine expression in septic/endotoxin shock and CAIA.

Indexed as

CD163endotoxin shockIL‐1βIL‐6rheumatoid arthritisseptic shock

Identifiers

PMID33005412
PMCPMC7518957
OpenAlexW3091086743

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.