Evidence map›Paper›PMID 10678917›Full record

ArticleInfection and immunity2000

Mechanisms of the proinflammatory response of endothelial cells to Candida albicans infection.

A S Orozco, X Zhou, S G Filler

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. IntestinalFrontiers in microbiology · 2022
    Article
  7. Review
  8. Review
  9. Article
  10. Pathogens (Basel, Switzerland) · 2019
    Review
  11. Journal of fungi (Basel, Switzerland) · 2019
    Article
  12. Article
  13. Experimental and therapeutic medicine · 2016
    Article
  14. Article
  15. Review
  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

3 authors at 1 institution in 1 country.

A S OrozcoSt. John's Cardiovascular Research Center, Division of Infectious Diseases, Department of Internal Medicine, Harbor-UCLA Research and Education Institute, Torrance, California 90502, USA.
X Zhou
S G Filler
University of California, Los Angeles · US

Funding

ZONA-FREE HAMSTER OVA ASSAY AS AN INDICATOR OF MALE FERTILITYM01RR000425 · NCRR · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI WANG, CHRISTINA C. · 1985 to 2011
$74.2M
PHOSPHOMANNOPROTEIN ADHESIN AS A VACCINE CANDIDATEP01AI037194 · NIAID · LA BIOMED RES INST/ HARBOR UCLA MED CTR · PI EDWARDS, JOHN E. · 1995 to 2003
$3.6M
CANDIDA ADHERENCE &PENETRATION--VASCULAR ENDOTHELIUMR01AI019990 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI EDWARDS, JOHN E · 1986 to 2009
$2.5M
NCRR NIH HHS M01 RR000425NIAID NIH HHS P01 AI037194NIAID NIH HHS P01 AI37194NIAID NIH HHS R01 AI019990NIAID NIH HHS R01 AI19990NIAID NIH HHS R29 AI04066
6 · The paper itself

Abstract

Endothelial cells can influence significantly the host inflammatory response against blood-borne microbial pathogens. Previously, we found that endothelial cells respond to in vitro infection with Candida albicans by secreting interleukin 8 (IL-8) and expressing E-selectin, intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1). We have now examined the mechanisms mediating this endothelial cell response. We determined that C. albicans stimulated endothelial cells to synthesize tumor necrosis factor alpha (TNF-alpha), which in turn induced these infected cells to secrete IL-8 and express E-selectin by an autocrine mechanism. Expression of VCAM-1 was mediated not only by TNF-alpha but also by IL-1alpha and IL-1beta, all of which were synthesized by endothelial cells in response to C. albicans. These three cytokines remained primarily cell associated rather than being secreted. Candidal induction of ICAM-1 expression was independent of TNF-alpha, IL-1alpha, and IL-1beta. These observations demonstrate that different proinflammatory endothelial cell responses to C. albicans are induced by distinct mechanisms. A clear understanding of these mechanisms is important for therapeutically modulating the endothelial cell response to C. albicans and perhaps other opportunistic pathogens that disseminate hematogenously.

Indexed as

Candida albicansEndothelium, VascularHumansInflammationInterleukin-1Platelet Activating FactorTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1Interleukin-1Platelet Activating FactorTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID10678917
PMCPMC97258
OpenAlexW2128473043

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.