Evidence map›Paper›PMID 25673319›Full record

ArticleGut2016

Ceramide-CD300f binding suppresses experimental colitis by inhibiting ATP-mediated mast cell activation.

Toshihiro Matsukawa, Kumi Izawa, Masamichi Isobe, Mariko Takahashi, Akie Maehara, Yoshinori Yamanishi, Ayako Kaitani, Ko Okumura, Takanori Teshima, Toshio Kitamura and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Gut, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 64 citations in OpenAlex.

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  15. Review
  16. CD300f immunoreceptor is associated with major depressive disorder and decreased microglial metabolic fitness.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  17. Structural basis for murine norovirus engagement of bile acids and the CD300lf receptor.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
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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

11 authors at 3 institutions in 1 country.

Toshihiro MatsukawaDepartment of Hematology, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido, Japan Division of Cellular Therapy, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Kumi IzawaDivision of Cellular Therapy, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan Atopy Research Center, Juntendo University School of Medicine, Tokyo, Japan.
Masamichi IsobeDivision of Cellular Therapy, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Mariko TakahashiDivision of Cellular Therapy, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Akie MaeharaDivision of Cellular Therapy, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yoshinori YamanishiDivision of Cellular Therapy, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Ayako KaitaniDivision of Cellular Therapy, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Ko OkumuraAtopy Research Center, Juntendo University School of Medicine, Tokyo, Japan.
Takanori TeshimaDepartment of Hematology, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido, Japan.
Toshio KitamuraDivision of Cellular Therapy, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan Division of Stem Cell Signaling, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Jiro KitauraDivision of Cellular Therapy, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan Atopy Research Center, Juntendo University School of Medicine, Tokyo, Japan.
The University of Tokyo · JPJuntendo University · JPHokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveExtracellular ATP mediates mast cell-dependent intestinal inflammation via P2X7 purinoceptors. We have previously shown that CD300f (also called the leucocyte mono-immunoglobulin-like receptor 3 (LMIR3)) suppresses immunoglobulin E-dependent and mast cell-dependent allergic responses by binding to ceramide. The aim of the present study was to clarify the role of ceramide-LMIR3 interaction in the development of IBD.

designThe dextran sodium sulfate (DSS)-induced colitis model was used in wild-type (WT), LMIR3(-/-), mast cell-deficient Kit(W-sh/W-sh), Kit(W-sh/W-sh)LMIR3(-/-) or Kit(W-sh/W-sh) mice engrafted with WT or LMIR3(-/-) bone marrow-derived mast cells (BMMCs). The severity of colitis was determined by clinical and histological criteria. Lamina propria cell populations were assessed by flow cytometry. Production of chemical mediators from lamina propria cells was measured by real-time reverse transcription PCR. Production of chemical mediators from ATP-stimulated BMMCs in the presence or absence of ceramide was measured by ELISA. The severity of DSS-induced colitis was assessed in mice given either an Fc fusion protein containing an extracellular domain of LMIR3, and anticeramide antibody, or ceramide liposomes.

resultsLMIR3 deficiency exacerbated DSS-induced colitis in mice. Kit(W-sh/W-sh) mice harbouring LMIR3(-/-) mast cells exhibited more severe colitis than those harbouring WT mast cells. Ceramide-LMIR3 interaction inhibited ATP-stimulated activation of BMMCs. DSS-induced colitis was aggravated by disrupting the ceramide-LMIR3 interaction, whereas it was suppressed by treating with ceramide liposomes.

conclusionsLMIR3-deficient colonic mast cells were pivotal in the exacerbation of DSS-induced colitis in LMIR3(-/-) mice. Ceramide liposomes attenuated DSS-induced colitis by inhibiting ATP-mediated activation of colonic mast cells through ceraimide-LMIR3 binding.

Indexed as

Adenosine TriphosphateAnimalsCeramidesColitisDisease Models, AnimalMast CellsMiceMice, Inbred C57BLReceptors, ImmunologicAdenosine TriphosphateCeramidesCLM-1 protein, mouseReceptors, ImmunologicEXPERIMENTAL COLITISGASTROINTESTINAL IMMUNE RESPONSEIBD MODELSINFLAMMATORY BOWEL DISEASE

Identifiers

PMID25673319
PMCPMC4853571
OpenAlexW2021093406

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.