Evidence map›Paper›PMID 15557648›Full record

ArticleInfection and immunity2004

Differential regulation of inflammatory cytokine secretion by human dendritic cells upon Chlamydia trachomatis infection.

Ana Gervassi, Mark R Alderson, Robert Suchland, Jean François Maisonneuve, Kenneth H Grabstein, Peter Probst

Abstract read
In one paragraph

Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

44 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Infection and immunity · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Frontiers in immunology · 2021
    Article
  10. Insights Into Host Cell Cytokines inFrontiers in immunology · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. BioMed research international · 2017
    Article
  17. Review
  18. Article
  19. Review
  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

6 authors at 2 institutions in 1 country.

Ana GervassiCorixa Corporation, 1900 9th Ave., Suite 1100, Seattle, WA 98101, USA.
Mark R Alderson
Robert Suchland
Jean François Maisonneuve
Kenneth H Grabstein
Peter Probst
Corixa Corporation · USUniversity of Washington · US

Funding

Diseases of Public Health Importance Training GrantT32AI007509 · NIAID · UNIVERSITY OF WASHINGTON · PI LUND, JENNIFER M · 1997 to 2024
$6.3M
NIAID NIH HHS T32 AI007509NIAID NIH HHS T32 AI 07509
6 · The paper itself

Abstract

Chlamydia trachomatis is an obligate intracellular gram-negative bacterium responsible for a wide spectrum of diseases in humans. Both genital and ocular C. trachomatis infections are associated with tissue inflammation and pathology. Dendritic cells (DC) play an important role in both innate and adaptive immune responses to microbial pathogens and are a source of inflammatory cytokines. To determine the potential contribution of DC to the inflammatory process, human DC were infected with C. trachomatis serovar E or L2. Both C. trachomatis serovars were found to infect and replicate in DC. Upon infection, DC up-regulated the expression of costimulatory (B7-1) and cell adhesion (ICAM-1) molecules. Furthermore, chlamydial infection induced the secretion of interleukin-1beta (IL-1beta), IL-6, IL-8, IL-12p70, IL-18, and tumor necrosis factor alpha (TNF-alpha). The mechanisms involved in Chlamydia-induced IL-1beta and IL-18 secretion differed from those of the other cytokines. Chlamydia-induced IL-1beta and IL-18 secretion required infection with viable bacteria and was associated with the Chlamydia-induced activation of caspase-1 in infected host cells. In contrast, TNF-alpha and IL-6 secretion did not require that the Chlamydia be viable, suggesting that there are at least two mechanisms involved in the Chlamydia-induced cytokine secretion in DC. Interestingly, an antibody to Toll-like receptor 4 inhibited Chlamydia-induced IL-1beta, IL-6, and TNF-alpha secretion. The data herein demonstrate that DC can be infected by human C. trachomatis serovars and that chlamydial components regulate the secretion of various cytokines in DC. Collectively, these data suggest that DC play a role in the inflammatory processes caused by chlamydial infections.

Indexed as

Caspase 1Cell Adhesion MoleculesChlamydia InfectionsChlamydia trachomatisCytokinesDendritic CellsEnzyme ActivationHumansInterleukin-1Interleukin-18Membrane GlycoproteinsReceptors, Cell SurfaceToll-Like Receptor 4Toll-Like ReceptorsCaspase 1Cell Adhesion MoleculesCytokinesInterleukin-1Interleukin-18Membrane GlycoproteinsReceptors, Cell SurfaceTLR4 protein, humanToll-Like Receptor 4Toll-Like Receptors

Identifiers

PMID15557648
PMCPMC529152
OpenAlexW2110794643

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.