Evidence map›Paper›PMID 26838052›Full record

ArticleMucosal immunology2016

Host innate inflammatory factors and staphylococcal protein A influence the duration of human Staphylococcus aureus nasal carriage.

A L Cole, G Muthukrishnan, C Chong, A Beavis, C R Eade, M P Wood, M G Deichen, A M Cole

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Nasal microbiome inhabitants with anti-Microbiology spectrum · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Surface Proteins ofMicrobiology spectrum · 2019
    Review
  15. Review
  16. Article
  17. Review
  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

8 authors at 3 institutions in 1 country.

A L ColeLaboratory of Innate Host Defense, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA.
G MuthukrishnanLaboratory of Innate Host Defense, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA.
C ChongLaboratory of Innate Host Defense, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA.
A BeavisLaboratory of Innate Host Defense, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA.
C R EadeLaboratory of Innate Host Defense, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA.
M P WoodLaboratory of Innate Host Defense, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA.
M G DeichenHealth Services, University of Central Florida, Orlando, Florida, USA.
A M ColeLaboratory of Innate Host Defense, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA.
University of Central Florida · USCenter for Infectious Disease Research · USUniversity of Rochester Medical Center · US

Funding

Nasal carriage of S. aureus: host-pathogen interactionsR01AI060753 · NIAID · UNIVERSITY OF CENTRAL FLORIDA · PI COLE, ALEXANDER MICHAEL · 2006 to 2010
$1.6M
NIAID NIH HHS R01 AI060753
6 · The paper itself

Abstract

Human Staphylococcus aureus (SA) nasal carriage provides a reservoir for the dissemination of infectious strains; however, factors regulating the establishment and persistence of nasal colonization are mostly unknown. We measured carriage duration and nasal fluid inflammatory markers after nasally inoculating healthy participants with their previously isolated SA strains. Out of 15 studies, 10 resulted in rapid clearance (9±6 days) that corresponded with upregulated chemokines, growth factors, and predominantly Th1-type cytokines, but not interleukin (IL)-17. Nasal SA persistence corresponded with elevated baseline levels of macrophage inflammatory protein-1β, IL-1β, and IL-6, no induction of inflammatory factors after inoculation, and decreased IL-1 receptor antagonist/IL-1β ratio. SA-expressed staphylococcal protein A (SpA) levels correlated positively with carriage duration. Competitive inoculation studies revealed that isogenic SpA knockout (ΔSpA) strains were cleared faster than wild type only in participants with upregulated inflammatory markers after inoculation. The remaining participants did not mount an inflammatory response and did not clear either strain. ΔSpA strains demonstrated lower growth rates in carrier nasal fluids and lower survival rates when incubated with neutrophils. Collectively, the presented studies identify innate immune effectors that cooperatively modulate nasal carriage duration, and confirm SpA as a bacterial codeterminant of SA nasal carriage.

Indexed as

Carrier StateImmunity, InnateBacterial AdhesionCytokinesFemaleGene Knockdown TechniquesHost-Pathogen InteractionsHumansInflammation MediatorsMaleMicrobial ViabilityMutationNasal MucosaNeutrophilsStaphylococcal InfectionsStaphylococcal Protein ACytokinesInflammation MediatorsStaphylococcal Protein A

Identifiers

PMID26838052
PMCPMC4972712
OpenAlexW2461691566

What OpenQuestion holds

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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.