Evidence map›Paper›PMID 23545303›Full record

ArticleInfection and immunity2013

Candida albicans-Staphylococcus aureus polymicrobial peritonitis modulates host innate immunity.

Brian M Peters, Mairi C Noverr

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
6.4field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 147 citations in OpenAlex.

  1. Article
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  6. bioRxiv : the preprint server for biology · 2025
    Article
  7. Frontiers in cellular and infection microbiology · 2025
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Journal of fungi (Basel, Switzerland) · 2023
    Article
  14. Article
  15. Article
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  17. Article
  18. Molecules (Basel, Switzerland) · 2022
    Review
  19. Article
  20. Article

27 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Brian M PetersDepartment of Oral and Craniofacial Biology, Dental School, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA.
Mairi C Noverr
Louisiana State University Health Sciences Center New Orleans · US

Funding

Host and microbial factors promoting synergistic mortality during polymicrobial intra-abdominal infections with Candida albicans and Staphylococcus aureusR01AI116025 · NIAID · TULANE UNIVERSITY OF LOUISIANA · PI NOVERR, MAIRI C · 2015 to 2019
$1.8M
NIAID NIH HHS R01 AI116025PHS HHS R01-A172406
6 · The paper itself

Abstract

Despite advances in medical device fabrication and antimicrobial treatment therapies, fungal-bacterial polymicrobial peritonitis remains a serious complication for surgery patients, those on peritoneal dialysis, and the critically ill. Using a murine model of peritonitis, we have demonstrated that monomicrobial infection with Candida albicans or Staphylococcus aureus is nonlethal. However, coinfection with these same doses leads to a 40% mortality rate and increased microbial burden in the spleen and kidney by day 1 postinfection. Using a multiplex enzyme-linked immunosorbent assay, we have also identified a unique subset of innate proinflammatory cytokines (interleukin-6, granulocyte colony-stimulating factor, keratinocyte chemoattractant, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1α) that are significantly increased during polymicrobial versus monomicrobial peritonitis, leading to increased inflammatory infiltrate into the peritoneum and target organs. Treatment of coinfected mice with the cyclooxygenase (COX) inhibitor indomethacin reduces the infectious burden, proinflammatory cytokine production, and inflammatory infiltrate while simultaneously preventing any mortality. Further experiments demonstrated that the immunomodulatory eicosanoid prostaglandin E2 (PGE2) is synergistically increased during coinfection compared to monomicrobial infection; indomethacin treatment also decreased elevated PGE2 levels. Furthermore, addition of exogenous PGE2 into the peritoneal cavity during infection overrode the protection provided by indomethacin and restored the increased mortality and microbial burden. Importantly, these studies highlight the ability of fungal-bacterial coinfection to modulate innate inflammatory events with devastating consequences to the host.

Indexed as

Immunity, InnateMethicillin-Resistant Staphylococcus aureusAnimalsAnti-Inflammatory Agents, Non-SteroidalCandida albicansCandidiasisCoinfectionEnzyme-Linked Immunosorbent AssayIndomethacinKidneyMicePeritonitisSpleenStaphylococcal InfectionsAnti-Inflammatory Agents, Non-SteroidalIndomethacin

Identifiers

PMID23545303
PMCPMC3676024
OpenAlexW2150774282

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.