Evidence map›Paper›PMID 16047468›Full record

ArticleDigestive diseases and sciences2005

Enhanced human beta-defensin-2 (hBD-2) expression by corticosteroids is independent of NF-kappaB in colonic epithelial cells (CaCo2).

T Witthöft, C S Pilz, K Fellermann, M Nitschke, E F Stange, D Ludwig

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. G.I. pros: Antimicrobial defense in the gastrointestinal tract.Seminars in cell & developmental biology · 2019
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Recombinant human beta 2-defensin fusion proteins as a tool to investigate defensin structure and function in small human intestinal tissue samples.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2012
    Article
  11. Article
  12. Toll-like receptors and corneal innate immunity.Current molecular medicine · 2006
    Review
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

6 authors at 3 institutions in 1 country.

T WitthöftDepartment of Medicine I, Division of Gastroenterology, University Hospital of Schleswig-Holstein, Campus Lübeck, Lübeck, Germany.
C S Pilz
K Fellermann
M Nitschke
E F Stange
D Ludwig
University of Lübeck · DERobert Bosch Hospital · DEUniversity Hospital Schleswig-Holstein · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Beta-defensins are small cationic peptides with antimicrobial properties that contribute to innate host defense. Unlike human beta-defensin-1 (hBD-1), which is produced constitutively, human beta-defensin-2 (hBD-2) is expressed after adequate stimulation by cytokines and/or bacterial endotoxins in epithelial tissue and mononuclear phagocytes but may be deficient in patients with Crohn's disease. To further elucidate the role of the intestinal epithelium in antimicrobial host defense, gene regulation of hBD-2 and the interaction with NF-kappaB were analyzed in a cell culture model. Human colonic epithelial cells (CaCo2) were stimulated by pro-inflammatory cytokines (IL-1beta, TNF-alpha, IF-gamma) to induce hBD-2 mRNA transcription. Interactions with NF-kappaB were analyzed using specific inhibitors (sulfasalazine, gliotoxine, dexamethasone) at different concentrations. Defensin mRNA expression was quantified by competitive RT-PCR and antibacterial capacity of supernatants was determined by an antimicrobial assay. HBD-2 mRNA transcription and antimicrobial activity of CaCo2 cells were induced by stimulation with pro-inflammatory cytokines. Induction was not inhibited by sulfasalazine or gliotoxine, whereas dexamethasone further enhanced both gene transcription and antimicrobial capacity. The lack of inhibition of induced hBD-2 expression by specific NF-kappaB antagonists suggests an additional pathway of activation, independent of NF-kappaB. The induction of hBD-2 expression in cytokine-stimulated CaCo2 cells by corticosteroids indicates further immunomodulatory ability of steroid hormones not yet understood.

Indexed as

Adrenal Cortex Hormonesbeta-DefensinsCaco-2 CellsColonColony Count, MicrobialCytokinesEpithelial CellsEscherichia coliGliotoxinHumansInterleukin-8NF-kappa BRNA, MessengerSulfasalazineAdrenal Cortex Hormonesbeta-DefensinsCytokinesDEFB1 protein, humanDEFB4A protein, humanGliotoxinInterleukin-8NF-kappa BRNA, MessengerSulfasalazine

Identifiers

PMID16047468
OpenAlexW2027987416

What OpenQuestion holds

Textmetadata
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.