Evidence map›Paper›PMID 28247863›Full record

ArticleCellular and molecular gastroenterology and hepatology2015

Anti-inflammatory Function of High-Density Lipoproteins via Autophagy of IκB Kinase.

Ragam Gerster, Jyrki J Eloranta, Martin Hausmann, Pedro A Ruiz, Jesus Cosin-Roger, Anne Terhalle, Urs Ziegler, Gerd A Kullak-Ublick, Arnold von Eckardstein, Gerhard Rogler

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

Article in Cellular and molecular gastroenterology and hepatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 29% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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  20. Natural polyphenols for the prevention of irritable bowel syndrome: molecular mechanisms and targets; a comprehensive review.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2019
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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 1 institution in 1 country.

Ragam GersterDivision of Gastroenterology and Hepatology, University Hospital Zurich, Zurich, Switzerland; Department of Clinical Pharmacology and Toxicology, University Hospital Zurich, Schlieren, Switzerland; Zurich Center of Integrative Human Physiology, University of Zurich, Zurich, Switzerland.
Jyrki J ElorantaDepartment of Clinical Pharmacology and Toxicology, University Hospital Zurich, Schlieren, Switzerland.
Martin HausmannDivision of Gastroenterology and Hepatology, University Hospital Zurich, Zurich, Switzerland.
Pedro A RuizDivision of Gastroenterology and Hepatology, University Hospital Zurich, Zurich, Switzerland.
Jesus Cosin-RogerDivision of Gastroenterology and Hepatology, University Hospital Zurich, Zurich, Switzerland; Departamento de Farmacología and CIBERehd, Facultad de Medicina, Universidad de Valencia, Valencia, Spain.
Anne TerhalleDivision of Gastroenterology and Hepatology, University Hospital Zurich, Zurich, Switzerland.
Urs ZieglerCentre for Microscopy and Image Analysis, University Hospital Zurich, Zurich, Switzerland.
Gerd A Kullak-UblickDepartment of Clinical Pharmacology and Toxicology, University Hospital Zurich, Schlieren, Switzerland; Zurich Center of Integrative Human Physiology, University of Zurich, Zurich, Switzerland.
Arnold von EckardsteinZurich Center of Integrative Human Physiology, University of Zurich, Zurich, Switzerland; Institute of Clinical Chemistry, University Hospital Zurich, Zurich, Switzerland.
Gerhard RoglerDivision of Gastroenterology and Hepatology, University Hospital Zurich, Zurich, Switzerland; Zurich Center of Integrative Human Physiology, University of Zurich, Zurich, Switzerland.
University Hospital of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsPlasma levels of high-density lipoprotein (HDL) cholesterol are frequently found decreased in patients with inflammatory bowel disease (IBD). Therefore, and because HDL exerts anti-inflammatory activities, we investigated whether HDL and its major protein component apolipoprotein A-I (apoA-I) modulate mucosal inflammatory responses in vitro and in vivo.

methodsThe human intestinal epithelial cell line T84 was used as the in vitro model for measuring the effects of HDL on the expression and secretion of tumor necrosis factor (TNF), interleukin-8 (IL-8), and intracellular adhesion molecule (ICAM). Nuclear factor-κB (NF-κB)-responsive promoter activity was studied by dual luciferase reporter assays. Mucosal damage from colitis induced by dextran sodium sulphate (DSS) and 2,4,6-trinitrobenzenesulfonic acid (TNBS) was scored by colonoscopy and histology in apoA-I transgenic (Tg) and apoA-I knockout (KO) and wild-type (WT) mice. Myeloperoxidase (MPO) activity and TNF and ICAM expression were determined in intestinal tissue samples. Autophagy was studied by Western blot analysis, immunofluorescence, and electron microscopy.

resultsHDL and apoA-I down-regulated TNF-induced mRNA expression of TNF, IL-8, and ICAM, as well as TNF-induced NF-κB-responsive promoter activity. DSS/TNBS-treated apoA-I KO mice displayed increased mucosal damage upon both colonoscopy and histology, increased intestinal MPO activity and mRNA expression of TNF and ICAM as compared with WT and apoA-I Tg mice. In contrast, apoA-I Tg mice showed less severe symptoms monitored by colonoscopy and MPO activity in both the DSS and TNBS colitis models. In addition, HDL induced autophagy, leading to recruitment of phosphorylated IκB kinase to the autophagosome compartment, thereby preventing NF-κB activation and induction of cytokine expression.

conclusionsTaken together, the in vitro and in vivo findings suggest that HDL and apoA-I suppress intestinal inflammation via autophagy and are potential therapeutic targets for the treatment of IBD.

Indexed as

3-MA, 3-methyl adenineApoA-I, apolipoprotein A-IApolipoprotein A-IAutophagyCD, Crohn’s diseaseDAPI, 4′,6-diamidino-2-phenylindoleDSS, dextran sodium sulphateEMSA, electrophoretic mobility shift assayHDL, high-density lipoproteinIBD, inflammatory bowel diseaseICAM, intracellular adhesion moleculeIL, interleukinInflammatory Bowel DiseaseKO, knockoutLC3II, light chain 3 IIMEICS, murine endoscopic index of colitis severityMPO, myeloperoxidasemTOR, the mammalian target of rapamycinNF-κBNF-κB, nuclear factor κBPBS, phosphate-buffered salinePFA, paraformaldehydePI-3, phosphatidylinositol-3p-IKK, phosphorylated IκB kinaseRT-PCR, real-time polymerase chain reactionsiRNA, small interfering RNATg, transgenicTNBS, 2,4,6-trinitrobenzenesulfonic acidTNF, tumor necrosis factorWT, wild type

Identifiers

PMID28247863
PMCPMC5301135
OpenAlexW2022344595

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.