Evidence map›Paper›PMID 23372642›Full record

ArticlePloS one2013

Activation of CD11b+ Kupffer cells/macrophages as a common cause for exacerbation of TNF/Fas-ligand-dependent hepatitis in hypercholesterolemic mice.

Hiroyuki Nakashima, Yoshiko Ogawa, Satoshi Shono, Manabu Kinoshita, Masahiro Nakashima, Atsushi Sato, Masami Ikarashi, Shuhji Seki

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

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  14. [The progress of studying the mechanisms of immune cells in the regulation of non-alcoholic fatty liver diseases].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2017
    Review
  15. Review
  16. Article
  17. Article
  18. Pathogenesis of Kupffer Cells in Cholestatic Liver Injury.The American journal of pathology · 2016
    Review
  19. Review
  20. 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

8 authors at 1 institution in 1 country.

Hiroyuki NakashimaDepartment of Immunology and Microbiology, National Defense Medical College, Tokorozawa, Saitama, Japan.
Yoshiko Ogawa
Satoshi Shono
Manabu Kinoshita
Masahiro Nakashima
Atsushi Sato
Masami Ikarashi
Shuhji Seki
National Defense Medical College · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have reported that the mouse hepatic injury induced by either α-galactosylceramide (α-GalCer) or bacterial DNA motifs (CpG-ODN) is mediated by the TNF/NKT cell/Fas-ligand (FasL) pathway. In addition, F4/80(+) Kupffer cells can be subclassified into CD68(+) subset with a phagocytosing capacity and CD11b(+) subset with a TNF-producing capacity. CD11b(+) subset increase if mice are fed high-fat and cholesterol diet (HFCD). The present study examined how a HFCD affects the function of NKT cells and F4/80(+) CD11b(+) subset and these hepatitis models. After the C57BL/6 mice received a HFCD, high-cholesterol diet (HCD), high-fat diet (HFD) and control diet (CD) for four weeks, the HFCD mice increased surface CD1d and intracellular TLR-9 expression by the CD11b(+) population compared to CD mice. Hepatic injury induced either by α-GalCer or CpG-ODN was more severe in HCD and HFCD mice compared to CD mice, which was in proportion to the serum TNF levels. In addition, liver cholesterol levels but not serum cholesterol levels nor liver triglyceride levels were involved in the aggravation of hepatitis. The FasL expression of NKT cells induced by both reagents was upregulated in HFCD mice. Furthermore, the liver mononuclear cells and purified F4/80(+) CD11b(+) subset from HFCD mice stimulated with either reagent in vitro produced a larger amount of TNF than did those from CD mice. Intracellular TNF production in F4/80(+) CD11b(+) cells was confirmed. The increased number of F4/80(+) CD11b(+) Kupffer cells/macrophages by HFCD and their enhanced TNF production thus play a pivotal role in TNF/NKT cell/FasL dependent hepatic injury.

Indexed as

AnimalsAntigens, CDAntigens, DifferentiationAntigens, Differentiation, MyelomonocyticCD11b AntigenCD68 MoleculeChemical and Drug Induced Liver InjuryCholesterolDiet, High-FatFas Ligand ProteinGalactosylceramidesGene Expression RegulationHypercholesterolemiaKiller Cells, NaturalKupffer CellsLiveralpha-galactosylceramideAntigens, CDAntigens, DifferentiationAntigens, Differentiation, MyelomonocyticCD11b AntigenCD68 MoleculeCD68 protein, mouseCholesterolCPG-oligonucleotideFas Ligand ProteinFasl protein, mouseGalactosylceramidesmonocyte-macrophage differentiation antigenOligodeoxyribonucleotidesTlr9 protein, mouseToll-Like Receptor 9Tumor Necrosis Factor-alpha

Identifiers

PMID23372642
PMCPMC3553091
OpenAlexW2075950996

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.