Evidence map›Paper›PMID 22504437›Full record

ArticleMicrobiology (Reading, England)2012

Mycoplasma polysaccharide protects against complement.

Jeffrey R Bolland, Warren L Simmons, James M Daubenspeck, Kevin Dybvig

Open access · greenAbstract read
In one paragraph

Article in Microbiology (Reading, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Microorganisms · 2025
    Review
  3. Review
  4. TheFrontiers in microbiology · 2022
    Review
  5. Review
  6. Virulence · 2020
    Article
  7. Article
  8. Article
  9. In vivo role of capsular polysaccharide in Mycoplasma mycoides.The Journal of infectious diseases · 2019
    Article
  10. O-linked protein glycosylation in Mycoplasma.Molecular microbiology · 2013
    Article
  11. Article
  12. Article
  13. 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

4 authors at 1 institution in 1 country.

Jeffrey R BollandDepartment of Microbiology, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Warren L SimmonsDepartment of Genetics, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
James M DaubenspeckDepartment of Genetics, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Kevin DybvigDepartment of Genetics, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
University of Alabama at Birmingham · US

Funding

Mechanisms of Mycoplasmal Disease PathogenesisR01AI063909 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DYBVIG, KEVIN F · 2005 to 2014
$3.0M
Tandemly Repetitive Proteins in MycoplasmasR01AI064848 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DYBVIG, KEVIN F · 2006 to 2010
$1.6M
MOLECULAR AND CELLULAR MICROBIAL PATHOGENESIST32AI007041 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BRILES, DAVID E · 1985 to 2008
$1.6M
NIAID NIH HHS AI63909NIAID NIH HHS AI64848NIAID NIH HHS R01 AI063909NIAID NIH HHS R01 AI064848NIAID NIH HHS T32 AI007041
6 · The paper itself

Abstract

Although they lack a cell wall, mycoplasmas do possess a glycocalyx. The interactions between the glycocalyx, mycoplasmal surface proteins and host complement were explored using the murine pathogen Mycoplasma pulmonis as a model. It was previously shown that the length of the tandem repeat region of the surface lipoprotein Vsa is associated with susceptibility to complement-mediated killing. Cells producing a long Vsa containing about 40 repeats are resistant to complement, whereas strains that produce a short Vsa of five or fewer repeats are susceptible. We show here that the length of the Vsa protein modulates the affinity of the M. pulmonis EPS-I polysaccharide for the mycoplasma cell surface, with more EPS-I being associated with mycoplasmas producing a short Vsa protein. An examination of mutants that lack EPS-I revealed that planktonic mycoplasmas were highly susceptible to complement killing even when the Vsa protein was long, demonstrating that both EPS-I and Vsa length contribute to resistance. In contrast, the mycoplasmas were resistant to complement even in the absence of EPS-I when the cells were encased in a biofilm.

Indexed as

AnimalsBacterial ProteinsComplement System ProteinsMembrane ProteinsMiceMicrobial ViabilityMycoplasma pulmonisPolysaccharides, BacterialBacterial ProteinsComplement System ProteinsMembrane ProteinsPolysaccharides, Bacterial

Identifiers

PMID22504437
PMCPMC3542145
OpenAlexW2127373850

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.