Evidence map›Paper›PMID 21377521›Full record

ArticleMicrobial pathogenesis2011

Exposure of Thomsen-Friedenreich antigen in Streptococcus pneumoniae infection is dependent on pneumococcal neuraminidase A.

Mamie T Coats, Trudy Murphy, James C Paton, Barry Gray, David E Briles

Abstract read
In one paragraph

Article in Microbial pathogenesis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. X-linked C1GALT1C1 mutation causes atypical hemolytic uremic syndrome.European journal of human genetics : EJHG · 2023
    Article
  5. Article
  6. Review
  7. Sialic acid and platelet count regulation: Implications in immune thrombocytopenia.Research and practice in thrombosis and haemostasis · 2022
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Successful treatment of aClinical kidney journal · 2019
    Article
  14. Review
  15. Role of Pneumococcal NanA Neuraminidase Activity in Peripheral Blood.Frontiers in cellular and infection microbiology · 2019
    Article
  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

5 authors at 4 institutions in 2 countries.

Mamie T CoatsDepartment of Microbiology, University of Alabama at Birmingham, 1530 3rd Ave South, Birmingham, AL 35294-2170, USA.
Trudy Murphy
James C Paton
Barry Gray
David E Briles
University of Alabama at Birmingham · USNational Center for Immunization and Respiratory Diseases · USPeoria campus of the University of Illinois System · USUniversity of Adelaide · AU

Funding

PspA: A Potential Pneumococcal Vaccine ComponentR01AI021548 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BRILES, DAVID E · 1985 to 2012
$6.0M
MOLECULAR AND CELLULAR MICROBIAL PATHOGENESIST32AI007041 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BRILES, DAVID E · 1985 to 2008
$1.6M
PspA mechanisms of humoral immunity, functional assays, and optimal vaccine constR56AI021548 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BRILES, DAVID E · 2014 to 2014
$543k
NIAID NIH HHS AI21548NIAID NIH HHS R01 AI021548NIAID NIH HHS R56 AI021548NIAID NIH HHS T32 AI007041
6 · The paper itself

Abstract

Pneumococcal hemolytic uremic syndrome is recognized in a small portion of otherwise healthy children who have or have recently had Streptococcus pneumoniae infections, including severe pneumonia, meningitis, and bacteremia. As in other types of hemolytic uremic syndrome (HUS), pneumococcal HUS is characterized by microangiopathic hemolytic anemia, and thrombocytopenia, usually with extensive kidney damage. Although not demonstrated in vivo, the pathogenesis of pneumococcal HUS has been attributed to the action pneumococcal neuraminidase exposing the usually cryptic Thomsen-Friedenreich antigen (T-antigen) on red blood cells (RBC), and kidney glomeruli. We evaluated the effect of pneumococcal infection on desialylation of RBC and glomeruli during pneumococcal infections in mice. Following intravenous infection with capsular type 19F pneumococci, CFU levels exceeding 1000 CFU/mL blood by the third day were significantly more likely to result in exposed T-antigen on RBC than lower levels of bacteremia. In a pneumonia model, significantly more T-antigen was exposed on RBC in mice treated with penicillin than in those receiving mock treatment. Utilizing mutant pneumococci, we demonstrated that neuraminidase A but not neuraminidase B was necessary for exposure of T-antigen on RBC in vivo. Thus, pneumococcal neuraminidase A is necessary for the exposure of T-antigen in vivo and treatment with penicillin increases this effect. Interestingly, NanA(-) pneumococci were found in the blood in higher numbers and caused more deaths than wild type, NanB(-), or the NanA(-)/NanB(-) pneumococci.

Indexed as

AnimalsAntigens, Tumor-Associated, CarbohydrateAntigens, Viral, TumorErythrocytesFemaleHemolytic-Uremic SyndromeKidneyMeningitis, PneumococcalMiceMice, Inbred CBANeuraminidasePneumococcal InfectionsPneumonia, BacterialStreptococcus pneumoniaeAntigens, Tumor-Associated, CarbohydrateAntigens, Viral, TumorNeuraminidaseThomsen-Friedenreich antigen

Identifiers

PMID21377521
PMCPMC3088309
OpenAlexW2015752702

What OpenQuestion holds

Textmetadata
LicenceTDM
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.