Evidence map›Paper›PMID 16040970›Full record

ArticleInfection and immunity2005

Invasive phenotype of Candida albicans affects the host proinflammatory response to infection.

C C Villar, H Kashleva, A P Mitchell, A Dongari-Bagtzoglou

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2005. 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
2.8field-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, 89 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Microbiota signatures associated with invasiveFrontiers in cellular and infection microbiology · 2023
    Article
  6. Review
  7. Frontiers in immunology · 2022
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Recurrent candidal intertrigo: challenges and solutions.Clinical, cosmetic and investigational dermatology · 2018
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  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

4 authors at 2 institutions in 1 country.

C C VillarDepartment of Periodontology, School of Dental Medicine, University of Connecticut, 263 Farmington Ave., Farmington, CT 06030-1710, USA.
H Kashleva
A P Mitchell
A Dongari-Bagtzoglou
University of Connecticut · USColumbia University · US

Funding

Oral Epithelial Cells, Candida and PMN ActivationR01DE013986 · NIDCR · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI Anna I Dongari-Bagtzoglou · 2000 to 2026
$9.2M
NIDCR NIH HHS 2R01 DE13986NIDCR NIH HHS R01 DE013986
6 · The paper itself

Abstract

Candida albicans is a major opportunistic pathogen in immunocompromised patients. Production of proinflammatory cytokines by host cells in response to C. albicans plays a critical role in the activation of immune cells and final clearance of the organism. Invasion of host cells and tissues is considered one of the virulence attributes of this organism. The purpose of this study was to investigate whether the ability of C. albicans to invade host cells and tissues affects the proinflammatory cytokine responses by epithelial and endothelial cells. In this study we used the invasion-deficient RIM101 gene knockout strain DAY25, the highly invasive strain SC5314, and highly invasive RIM101-complemented strain DAY44 to compare the proinflammatory cytokine responses by oral epithelial or endothelial cells. Using a high-throughput approach, we found both qualitative and quantitative differences in the overall inflammatory responses to C. albicans strains with different invasive potentials. Overall, the highly invasive strains triggered higher levels of proinflammatory cytokines in host cells than the invasion-deficient mutant triggered. Significant differences compared to the attenuated mutant were noted in interleukin-1alpha (IL-1alpha), IL-6, IL-8, and tumor necrosis factor alpha in epithelial cells and in IL-6, growth-related oncogene, IL-8, monocyte chemoattractant protein 1 (MCP-1), MCP-2, and granulocyte colony-stimulating factor in endothelial cells. Our results indicate that invasion of host cells and tissues by C. albicans enhances the host proinflammatory response to infection.

Indexed as

Candida albicansCandidiasisCytokinesDNA-Binding ProteinsEndotheliumFungal ProteinsHumansInflammationMouth MucosaTissue EngineeringCytokinesDNA-Binding ProteinsFungal ProteinsRIM101 protein, Candida albicans

Identifiers

PMID16040970
PMCPMC1201248
OpenAlexW2099005279

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.