Evidence map›Paper›PMID 20434582›Full record

ArticleMicrobes and infection2010

Chlamydial infection of monocytes stimulates IL-1beta secretion through activation of the NLRP3 inflammasome.

Ali A Abdul-Sater, Najwane Saïd-Sadier, Eduardo V Padilla, David M Ojcius

Open access · greenAbstract read
In one paragraph

Article in Microbes and infection, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

52 citing papers in PubMed, 82 citations in OpenAlex.

  1. Live Imaging of Ions in Cells Infected with Chlamydia trachomatis.Methods in molecular biology (Clifton, N.J.) · 2027
    Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
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  8. Article
  9. Article
  10. Review
  11. Article
  12. Microorganisms · 2021
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Frontiers in aging neuroscience · 2018
    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

4 authors at 2 institutions in 2 countries.

Ali A Abdul-Sater *Health Sciences Research Institute and School of Natural Sciences, University of California, Merced, CA 95343, USA.
Najwane Saïd-Sadier *Health Sciences Research Institute and School of Natural Sciences, University of California, Merced, CA 95343, USA.
Eduardo V PadillaHealth Sciences Research Institute and School of Natural Sciences, University of California, Merced, CA 95343, USA.
David M OjciusHealth Sciences Research Institute and School of Natural Sciences, University of California, Merced, CA 95343, USA.
University of California, Merced · USUniversité Paris Cité · FR

Funding

Novel ways to prevent upper GT infectionR01AI079004 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KELLY, KATHLEEN A. · 2010 to 2014
$1.9M
The Inflammasome in Gingival Epithelial Cells During Porphyromonas InfectionR01DE019444 · NIDCR · UNIVERSITY OF CALIFORNIA, MERCED · PI OJCIUS, DAVID MARCELO · 2009 to 2012
$1.3M
NIAID NIH HHS R01 AI079004NIDCR NIH HHS R01 DE019444
6 · The paper itself

Abstract

Chlamydia trachomatis infections represent the leading cause of bacterial sexually-transmitted disease in the United States and can cause serious tissue damage leading to infertility and ectopic pregnancies in women. Inflammation and hence the innate immune response to chlamydial infection contributes significantly to tissue damage, particularly by secreting proinflammatory cytokines such as interleukin (IL)-1beta from monocytes, macrophages and dendritic cells. Here we demonstrate that C. trachomatis or Chlamydia muridarum infection of a monocytic cell line leads to caspase-1 activation and IL-1beta secretion through a process requiring the NLRP3 inflammasome. Thus, secretion of IL-1beta decreased significantly when cells were depleted of NLRP3 or treated with the anti-inflammatory inhibitors parthenolide or Bay 11-7082, which inhibit inflammasomes and the transcription factor NF-kappaB. As for other infections causing NRLP3 inflammasome assembly, caspase-1 activation in monocytes is triggered by potassium efflux and reactive oxygen species production. However, anti-oxidants inhibited IL-1beta secretion only partially. Atypically for a bacterial infection, caspase-1 activation during chlamydial infection also involves partially the spleen tyrosine kinase (Syk), which is usually associated with a pathogen recognition receptor for fungal pathogens. Secretion of IL-1beta during infection by many bacteria requires both microbial products from the pathogen and an exogenous danger signal, but chlamydial infection provides both the pathogen-associated molecular patterns and danger signals necessary for IL-1beta synthesis and its secretion from human monocytes. Use of inhibitors that target the inflammasome in animals should therefore dampen inflammation during chlamydial infection.

Indexed as

Carrier ProteinsCaspase 1Cell LineChlamydia muridarumChlamydia trachomatisEnzyme InhibitorsHumansInterleukin-1betaMonocytesNitrilesNLR Family, Pyrin Domain-Containing 3 ProteinSesquiterpenesSulfones3-(4-methylphenylsulfonyl)-2-propenenitrileCarrier ProteinsCaspase 1Enzyme InhibitorsInterleukin-1betaNitrilesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanparthenolideSesquiterpenesSulfones

Identifiers

PMID20434582
PMCPMC4074088
OpenAlexW2051714701

What OpenQuestion holds

Textmetadata
LicenceTDM
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.