Evidence map›Paper›PMID 20145101›Full record

ArticleInfection and immunity2010

Examination of type IV pilus expression and pilus-associated phenotypes in Kingella kingae clinical isolates.

Thomas E Kehl-Fie, Eric A Porsch, Pablo Yagupsky, Elizabeth A Grass, Caroline Obert, Daniel K Benjamin, Joseph W St Geme

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Microorganisms · 2022
    Article
  3. Microorganisms · 2022
    Review
  4. Pharyngeal Colonization byMicroorganisms · 2022
    Review
  5. Microorganisms · 2022
    Article
  6. Pathogenic determinants ofFrontiers in pediatrics · 2022
    Review
  7. Fulminant Infective Endocarditis Due toFrontiers in pediatrics · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Kingella kingae: carriage, transmission, and disease.Clinical microbiology reviews · 2015
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

7 authors at 4 institutions in 2 countries.

Thomas E Kehl-FieDepartment of Molecular Microbiology, Washington University School of Medicine, 660 S Euclid Ave, St. Louis, Missouri 63110, USA.
Eric A Porsch
Pablo Yagupsky
Elizabeth A Grass
Caroline Obert
Daniel K Benjamin
Joseph W St Geme
Ben-Gurion University of the Negev · ILClinical Research Institute · USSt. Jude Children's Research Hospital · USWashington University in St. Louis · US

Funding

TRAINING PROGRAM IN CELLULAR AND MOLECULAR BIOLOGYT32GM007067 · NIGMS · WASHINGTON UNIVERSITY · PI TRUE-KROB, HEATHER L · 1985 to 2020
$20.4M
NIGMS NIH HHS T32 GM007067NIGMS NIH HHS T32-GM07067
6 · The paper itself

Abstract

Kingella kingae is a gram-negative bacterium that is being recognized increasingly as a cause of septic arthritis and osteomyelitis in young children. Previous work established that K. kingae expresses type IV pili that mediate adherence to respiratory epithelial and synovial cells. PilA1 is the major pilus subunit in K. kingae type IV pili and is essential for pilus assembly. To develop a better understanding of the role of K. kingae type IV pili during colonization and invasive disease, we examined a collection of clinical isolates for pilus expression and in vitro adherence. In addition, in a subset of isolates we performed nucleotide sequencing to assess the level of conservation of PilA1. The majority of respiratory and nonendocarditis blood isolates were piliated, while the majority of joint fluid, bone, and endocarditis blood isolates were nonpiliated. The piliated isolates formed either spreading/corroding or nonspreading/noncorroding colonies and were uniformly adherent, while the nonpiliated isolates formed domed colonies and were nonadherent. PilA1 sequence varied significantly from strain to strain, resulting in substantial variability in antibody reactivity. These results suggest that type IV pili may confer a selective advantage on K. kingae early in infection and a selective disadvantage on K. kingae at later stages in the pathogenic process. We speculate that PilA1 is immunogenic during natural infection and undergoes antigenic variation to escape the immune response.

Indexed as

Bacterial AdhesionGene Expression Regulation, BacterialAntibodies, BacterialArthritis, InfectiousBacterial ProteinsCarrier StateDNA, BacterialFimbriae, BacterialFimbriae ProteinsHumansKingella kingaeMolecular Sequence DataNeisseriaceae InfectionsOsteomyelitisPhenotypePolymorphism, GeneticAntibodies, BacterialBacterial ProteinsDNA, BacterialFimbriae Proteins

Identifiers

PMID20145101
PMCPMC2849430
OpenAlexW2166923112

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.