Evidence map›Paper›PMID 19787068›Full record

ArticlePloS one2009

Lipid alterations in experimental murine colitis: role of ceramide and imipramine for matrix metalloproteinase-1 expression.

Jessica Bauer, Gerhard Liebisch, Claudia Hofmann, Christian Huy, Gerd Schmitz, Florian Obermeier, Jürgen Bock

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed, 44 citations in OpenAlex.

  1. CD39 and CD161 modulate Th17 responses in Crohn's disease.Journal of immunology (Baltimore, Md. : 1950) · 2014
    Trial
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  9. Fat of the Gut: Epithelial Phospholipids in Inflammatory Bowel Diseases.International journal of molecular sciences · 2021
    Review
  10. Article
  11. G2A Signaling Dampens Colitic Inflammation via Production of IFN-γ.Journal of immunology (Baltimore, Md. : 1950) · 2016
    Article
  12. Article
  13. Article
  14. Article
  15. PPARα-dependent exacerbation of experimental colitis by the hypolipidemic drug fenofibrate.American journal of physiology. Gastrointestinal and liver physiology · 2014
    Article
  16. Article
  17. Review
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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

7 authors.

Jessica BauerDepartment of Internal Medicine I, University Medical Center, Regensburg, Germany.
Gerhard Liebisch
Claudia Hofmann
Christian Huy
Gerd Schmitz
Florian Obermeier
Jürgen Bock

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDietary lipids or pharmacologic modulation of lipid metabolism are potential therapeutic strategies in inflammatory bowel disease (IBD). Therefore, we analysed alterations of bioactive lipids in experimental models of colitis and examined the functional consequence of the second messenger ceramide in inflammatory pathways leading to tissue destruction. METHODOLOGY/PRINCIPAL

findingsChronic colitis was induced by dextran-sulphate-sodium (DSS) or transfer of CD4(+)CD62L(+) cells into RAG1(-/-)-mice. Lipid content of isolated murine intestinal epithelial cells (IEC) was analysed by tandem mass spectrometry. Concentrations of MMP-1 in supernatants of Caco-2-IEC and human intestinal fibroblasts from patients with ulcerative colitis were determined by ELISA. Imipramine was used for pharmacologic inhibition of acid sphingomyelinase (ASM). Ceramide increased by 71% in chronic DSS-induced colitis and by 159% in the transfer model of colitis. Lysophosphatidylcholine (LPC) decreased by 22% in both models. No changes were detected for phosphatidylcholine. Generation of ceramide by exogenous SMase increased MMP-1-protein production of Caco-2-IEC up to 7-fold. Inhibition of ASM completely abolished the induction of MMP-1 by TNF or IL-1beta in Caco-2-IEC and human intestinal fibroblasts. CONCLUSIONS/SIGNIFICANCE: Mucosal inflammation leads to accumulation of ceramide and decrease of LPC in the intestinal epithelium. One aspect of ceramide generation is an increase of MMP-1. Induction of MMP-1 by TNF or IL-1beta is completely blocked by inhibition of ASM with imipramine. Therefore, inhibition of ASM may offer a treatment strategy to reduce MMP-1 expression and tissue destruction in inflammatory conditions.

Indexed as

Gene Expression Regulation, EnzymologicAnimalsCaco-2 CellsCeramidesColitisHumansImipramineInterleukin-1betaLipid MetabolismLipidsL-SelectinLysophosphatidylcholinesMaleMatrix Metalloproteinase 1MiceMice, Inbred BALB Cacid sphingomyelinase-1CeramidesImipramineInterleukin-1betaLipidsL-SelectinLysophosphatidylcholinesMatrix Metalloproteinase 1Sphingomyelin PhosphodiesteraseTumor Necrosis Factor-alpha

Identifiers

PMID19787068
PMCPMC2749204
OpenAlexW1972100892

What OpenQuestion holds

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LicenceCC BY
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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.