Evidence map›Paper›PMID 22174882›Full record

ArticlePloS one2011

Streptococcus pneumoniae in biofilms are unable to cause invasive disease due to altered virulence determinant production.

Carlos J Sanchez, Nikhil Kumar, Anel Lizcano, Pooja Shivshankar, Julie C Dunning Hotopp, James H Jorgensen, Hervé Tettelin, Carlos J Orihuela

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

75 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Carbon source-dependent capsule thickness regulation inFrontiers in cellular and infection microbiology · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

15 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

8 authors at 2 institutions in 1 country.

Carlos J SanchezDepartment of Microbiology and Immunology, The University of Texas Health Science Center at San Antonio, Texas, United States of America.
Nikhil Kumar
Anel Lizcano
Pooja Shivshankar
Julie C Dunning Hotopp
James H Jorgensen
Hervé Tettelin
Carlos J Orihuela
The University of Texas Health Science Center at San Antonio · USUniversity of Maryland, Baltimore · US

Funding

Institutional Research Training GrantT32DE014318 · NIDCR · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Kenneth M Hargreaves · 2002 to 2026
$12.1M
Mechanism of PsrP mediated adhesionR01AI078972 · NIAID · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ORIHUELA, CARLOS J · 2009 to 2013
$1.3M
NIAID NIH HHS AI078972NIAID NIH HHS R01 AI078972NIDCR NIH HHS DE14318NIDCR NIH HHS T32 DE014318
6 · The paper itself

Abstract

It is unclear whether Streptococcus pneumoniae in biofilms are virulent and contribute to development of invasive pneumococcal disease (IPD). Using electron microscopy we confirmed the development of mature pneumococcal biofilms in a continuous-flow-through line model and determined that biofilm formation occurred in discrete stages with mature biofilms composed primarily of dead pneumococci. Challenge of mice with equal colony forming units of biofilm and planktonic pneumococci determined that biofilm bacteria were highly attenuated for invasive disease but not nasopharyngeal colonization. Biofilm pneumococci of numerous serotypes were hyper-adhesive and bound to A549 type II pneumocytes and Detroit 562 pharyngeal epithelial cells at levels 2 to 11-fold greater than planktonic counterparts. Using genomic microarrays we examined the pneumococcal transcriptome and determined that during biofilm formation S. pneumoniae down-regulated genes involved in protein synthesis, energy production, metabolism, capsular polysaccharide (CPS) production, and virulence. We confirmed these changes by measuring CPS by ELISA and immunoblotting for the toxin pneumolysin and the bacterial adhesins phosphorylcholine (ChoP), choline-binding protein A (CbpA), and Pneumococcal serine-rich repeat protein (PsrP). We conclude that biofilm pneumococci were avirulent due to reduced CPS and pneumolysin production along with increased ChoP, which is known to bind C-reactive protein and is opsonizing. Likewise, biofilm pneumococci were hyper-adhesive due to selection for the transparent phase variant, reduced CPS, and enhanced production of PsrP, CbpA, and ChoP. These studies suggest that biofilms do not directly contribute to development of IPD and may instead confer a quiescent mode of growth during colonization.

Indexed as

AnimalsAnti-Infective AgentsBacterial AdhesionBacterial CapsulesBacterial ProteinsBiofilmsCell LineGene Expression Regulation, BacterialHumansMiceMicrobial Sensitivity TestsPhenotypePlanktonPneumococcal InfectionsReproducibility of ResultsStreptococcus pneumoniaeAnti-Infective AgentsBacterial ProteinsCbpA protein, bacteriaplY protein, Streptococcus pneumoniaeStreptolysinsVirulence Factors

Identifiers

PMID22174882
PMCPMC3234282
OpenAlexW2066496579

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.