Evidence map›Paper›PMID 16622206›Full record

ArticleInfection and immunity2006

Campylobacter jejuni induces maturation and cytokine production in human dendritic cells.

Lan Hu, Mechelle D Bray, Manuel Osorio, Dennis J Kopecko

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
11.4field-weighted citation impact, top 1% 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

49 citing papers in PubMed, 99 citations in OpenAlex.

  1. Trial
  2. Lack of homologous protection against Campylobacter jejuni CG8421 in a human challenge model.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2013
    Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Campylobacter coli strains from Brazil can invade phagocytic and epithelial cells and induce IL-8 secretion.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2021
    Article
  11. Article
  12. Contribution ofFrontiers in microbiology · 2020
    Article
  13. Human Immunity AgainstImmune network · 2019
    Review
  14. Article
  15. Protease Activity ofFrontiers in cellular and infection microbiology · 2019
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

4 authors at 1 institution in 1 country.

Lan HuLaboratory of Enteric and Sexually Transmitted Diseases, Center for Biologics Evaluation and Research, Food and Drug Administration, 29 Lincoln Drive, NIH Campus, Bethesda, MD 20892, USA.
Mechelle D Bray
Manuel Osorio
Dennis J Kopecko
Center for Biologics Evaluation and Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Campylobacter jejuni is a leading bacterial cause of human diarrheal disease in both developed and developing nations. Colonic mucosal invasion and the resulting host inflammatory responses are thought to be the key contributing factors to the dysenteric form of this disease. Dendritic cells (DCs) play an important role in both the innate and adaptive immune responses to microbial infection. In this study, the interaction between human monocyte-derived dendritic cells and C. jejuni was studied. We found that C. jejuni was readily internalized by DCs over a 2-h period. However, after a prolonged infection period (24 or 48 h) with C. jejuni, only a few viable bacteria remained intracellularly. Minimal cytotoxicity of C. jejuni to dendritic cells was observed. C. jejuni induced the maturation of dendritic cells over 24 h, as indicated by up-regulation of cell surface marker proteins CD40, CD80, and CD86. In addition, Campylobacter-infected DCs triggered activation of NF-kappaB and significantly stimulated production of interleukin-1beta (IL-1beta), IL-6, IL-8, IL-10, IL-12, gamma interferon, and tumor necrosis factor alpha (TNF-alpha) compared to uninfected DCs. Active bacterial invasion of DCs was not necessary for the induction of these cytokines, as heat-killed C. jejuni stimulated similar levels of cytokine production as live bacteria. Purified lipooligosaccharide of C. jejuni appears to be the major stimulant for the increased production of cytokines by DCs. Taken together, these data indicate that during infection, Campylobacter triggers an innate inflammatory response through increased production of IL-1beta, IL-6, IL-8, and TNF-alpha and initiates a Th1-polarized adaptive immune response as predicted from the high level of production of IL-12.

Indexed as

Campylobacter jejuniCytokinesDendritic CellsHumansLipopolysaccharidesNF-kappa BCytokineslipid-linked oligosaccharidesLipopolysaccharidesNF-kappa B

Identifiers

PMID16622206
PMCPMC1459697
OpenAlexW2098157455

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.