Evidence map›Paper›PMID 19664152›Full record

ArticleClinical and experimental immunology2009

Exaggerated inflammatory response of primary human myeloid dendritic cells to lipopolysaccharide in patients with inflammatory bowel disease.

D C Baumgart, S Thomas, I Przesdzing, D Metzke, C Bielecki, S M Lehmann, S Lehnardt, Y Dörffel, A Sturm, A Scheffold and 2 more

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 96 citations in OpenAlex.

  1. Trial
  2. Article
  3. TET1 deficiency amplifies macrophage inflammatory signaling associated with Crohn's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  4. Review
  5. Review
  6. The Pathogenesis of Inflammatory Bowel Diseases.The Surgical clinics of North America · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
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  14. Article
  15. Review
  16. Review
  17. Bacterial Translocation as Inflammatory Driver in Crohn's Disease.Frontiers in cell and developmental biology · 2021
    Review
  18. Article
  19. Article
  20. 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

12 authors at 2 institutions in 2 countries.

D C BaumgartDepartment of Medicine, Division of Gastroenterology and Hepatology, Charité Medical School of the Humboldt-University of Berlin, D-13344 Berlin, Germany. daniel.baumgart@charite.de
S Thomas
I Przesdzing
D Metzke
C Bielecki
S M Lehmann
S Lehnardt
Y Dörffel
A Sturm
A Scheffold
J Schmitz
A Radbruch
German Rheumatism Research Centre · DEHumboldt State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) results from a breakdown of tolerance towards the indigenous flora in genetically susceptible hosts. Failure of dendritic cells (DC) to interpret molecular microbial patterns appropriately when directing innate and adaptive immune responses is conceivable. Primary (conventional, non-monocyte generated) CD1c(+)CD11c(+)CD14(-)CD16(-)CD19(-) myeloid blood or mucosal dendritic cells (mDC) from 76 patients with Crohn's disease (CD) or ulcerative colitis (UC) in remission, during flare-ups (FU) and 76 healthy or non-IBD controls were analysed by fluorescence activated cell sorter (FACS) flow cytometry and real-time polymerase chain reaction. Cytokine secretion of freshly isolated, cultured and lipopolysaccharide (LPS)-stimulated highly purified mDC (purity >95%) was assessed using cytometric bead arrays (CBA). More cultured and stimulated circulating mDC express CD40 in IBD patients. Stimulated circulating mDC from IBD patients secrete significantly more tumour necrosis factor (TNF)-alpha and interleukin (IL)-8. Toll-like receptor (TLR)-4 expression by mDC was higher in remission and increased significantly in flaring UC and CD patients compared with remission (P < 0.05) and controls (P < 0.001). Fluorochrome-labelled LPS uptake by mDC was evaluated at different time-points over 24 h by measuring mean fluorescence intensity (MFI). Circulating mDC from IBD patients take up more LPS and the uptake begins earlier compared with controls (P < 0.05 in CD-FU and UC-FU at 24 h). The frequency of mucosal mDC (P < 0.05) and the number of CD40 expressing mucosal mDC is significantly greater in UC and CD compared with non-IBD controls (P < 0.001 versus P < 0.01, respectively). Our data suggest an aberrant LPS response of mDC in IBD patients, resulting in an inflammatory phenotype and possibly intestinal homing in acute flares.

Indexed as

Acute DiseaseAdultAntigen PresentationCase-Control StudiesCD40 AntigensCells, CulturedColitis, UlcerativeCrohn DiseaseDendritic CellsFemaleFlow CytometryHumansImmunizationImmunophenotypingInflammationInflammatory Bowel DiseasesCD40 AntigensLipopolysaccharidesRNA, MessengerTLR2 protein, humanTLR4 protein, humanToll-Like Receptor 2Toll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID19664152
PMCPMC2745038
OpenAlexW1596764898

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.