Evidence map›Paper›PMID 27810309›Full record

ArticleEBioMedicine2016

Commensal Microbe-specific Activation of B2 Cell Subsets Contributes to Atherosclerosis Development Independently of Lipid Metabolism.

Lin Chen, Tomoaki Ishigami, Rie Nakashima-Sasaki, Tabito Kino, Hiroshi Doi, Shintaro Minegishi, Satoshi Umemura

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Lin ChenDepartment of Medical Science and Cardio-Renal Medicine, Yokohama City University, Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, Kanagawa, Japan.
Tomoaki IshigamiDepartment of Medical Science and Cardio-Renal Medicine, Yokohama City University, Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, Kanagawa, Japan. Electronic address: tommmish@hotmail.com.
Rie Nakashima-SasakiDepartment of Medical Science and Cardio-Renal Medicine, Yokohama City University, Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, Kanagawa, Japan.
Tabito KinoDepartment of Medical Science and Cardio-Renal Medicine, Yokohama City University, Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, Kanagawa, Japan.
Hiroshi DoiDepartment of Medical Science and Cardio-Renal Medicine, Yokohama City University, Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, Kanagawa, Japan.
Shintaro MinegishiDepartment of Medical Science and Cardio-Renal Medicine, Yokohama City University, Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, Kanagawa, Japan.
Satoshi UmemuraDepartment of Medical Science and Cardio-Renal Medicine, Yokohama City University, Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, Kanagawa, Japan.
Yokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The relation between B2 cells and commensal microbes during atherosclerosis remains largely unexplored. Here we show that under hyperlipidemic conditions intestinal microbiota resulted in recruitment and ectopic activation of B2 cells in perivascular adipose tissue, followed by an increase in circulating IgG, promoting disease development. In contrast, disruption of the intestinal microbiota by a broad-spectrum antibiotic cocktail (AVNM) led to the attenuation of atherosclerosis by suppressing B2 cells, despite the persistence of serum lipid abnormalities. Furthermore, pharmacological depletion of B2 cells with an anti-B2-cell surface CD23 antibody also attenuated commensal microbe-induced atherosclerosis. Moreover, expression analysis of TLR-signaling-related genes in the activated B2 cell subsets, assessed using the Toll-Like Receptor Signaling Pathway RT2 Profiler PCR Array, confirmed activation of the B2-cell autoantibody-production axis, which was associated with an increased capacity of B2 cells to bind to intestinal microbiota. Together, our findings reveal the critical role of commensal microbe-specific activation of B2 cells in the development of atherogenesis through lipid metabolism-independent mechanisms.

Indexed as

Lipid MetabolismAnimalsAnti-Bacterial AgentsAtherosclerosisB-Lymphocyte SubsetsCluster AnalysisCytokinesDisease Models, AnimalGastrointestinal MicrobiomeGene ExpressionGene Expression ProfilingInflammation MediatorsLymphocyte ActivationMaleMiceMice, KnockoutAnti-Bacterial AgentsCytokinesInflammation MediatorsToll-Like ReceptorsAtherosclerosisB2 cellInflammationIntestinal microbiotaTLR signaling

Identifiers

PMID27810309
PMCPMC5264349
OpenAlexW2538637593

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.