Evidence map›Paper›PMID 28095507›Full record

ArticlePloS one2017

Choline Deficiency Causes Colonic Type II Natural Killer T (NKT) Cell Loss and Alleviates Murine Colitis under Type I NKT Cell Deficiency.

Shintaro Sagami, Yoshitaka Ueno, Shinji Tanaka, Akira Fujita, Hiroaki Niitsu, Ryohei Hayashi, Hideyuki Hyogo, Takao Hinoi, Yasuhiko Kitadai, Kazuaki Chayama

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

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  9. [Research progress on composite animal models of inflammatory bowel disease based on gene knockout].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018
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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

10 authors at 5 institutions in 1 country.

Shintaro SagamiDepartment of Medicine and Molecular Science, Hiroshima University, Hiroshima, Japan.
Yoshitaka UenoDepartment of Endoscopy, Hiroshima University Hospital, Hiroshima, Japan.
Shinji TanakaDepartment of Endoscopy, Hiroshima University Hospital, Hiroshima, Japan.
Akira FujitaDepartment of Medicine and Molecular Science, Hiroshima University, Hiroshima, Japan.
Hiroaki NiitsuDepartment of Gastroenterological and Transplant Surgery, Applied Life Sciences, Institute of Biomedical & Health Sciences, Hiroshima University, Hiroshima, Japan.
Ryohei HayashiDepartment of Endoscopy, Hiroshima University Hospital, Hiroshima, Japan.
Hideyuki HyogoDepartment of Gastroenterology, Hiroshima General Hospital, Hiroshima, Japan.
Takao HinoiDepartment of Gastroenterological and Transplant Surgery, Applied Life Sciences, Institute of Biomedical & Health Sciences, Hiroshima University, Hiroshima, Japan.
Yasuhiko KitadaiDepartment of Life Sciences, Prefectural University of Hiroshima, Hiroshima, Japan.
Kazuaki ChayamaDepartment of Medicine and Molecular Science, Hiroshima University, Hiroshima, Japan.
Hiroshima University · JPHiroshima University Hospital · JPHiroshima General Hospital · JPKure Medical Center · JPPrefectural University of Hiroshima · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Serum levels of choline and its derivatives are lower in patients with inflammatory bowel disease (IBD) than in healthy individuals. However, the effect of choline deficiency on the severity of colitis has not been investigated. In the present study, we investigated the role of choline deficiency in dextran sulfate sodium (DSS)-induced colitis in mice. Methionine-choline-deficient (MCD) diet lowered the levels of type II natural killer T (NKT) cells in the colonic lamina propria, peritoneal cavity, and mesenteric lymph nodes, and increased the levels of type II NKT cells in the livers of wild-type B6 mice compared with that in mice fed a control (CTR) diet. The gene expression pattern of the chemokine receptor CXCR6, which promotes NKT cell accumulation, varied between colon and liver in a manner dependent on the changes in the type II NKT cell levels. To examine the role of type II NKT cells in colitis under choline-deficient conditions, we assessed the severity of DSS-induced colitis in type I NKT cell-deficient (Jα18-/-) or type I and type II NKT cell-deficient (CD1d-/-) mice fed the MCD or CTR diets. The MCD diet led to amelioration of inflammation, decreases in interferon (IFN)-γ and interleukin (IL)-4 secretion, and a decrease in the number of IFN-γ and IL-4-producing NKT cells in Jα18-/- mice but not in CD1d-/- mice. Finally, adaptive transfer of lymphocytes with type II NKT cells exacerbated DSS-induced colitis in Jα18-/- mice with MCD diet. These results suggest that choline deficiency causes proinflammatory type II NKT cell loss and alleviates DSS-induced colitis. Thus, inflammation in DSS-induced colitis under choline deficiency is caused by type II NKT cell-dependent mechanisms, including decreased type II NKT cell and proinflammatory cytokine levels.

Indexed as

Disease Models, AnimalAnimalsCholine DeficiencyColitisCytokinesDextran SulfateInflammationInterferon-gammaMaleMiceMice, Inbred C57BLNatural Killer T-CellsCytokinesDextran SulfateInterferon-gamma

Identifiers

PMID28095507
PMCPMC5241147
OpenAlexW2576359618

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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.