Evidence map›Paper›PMID 14500494›Full record

ArticleInfection and immunity2003

The Vsa proteins modulate susceptibility of Mycoplasma pulmonis to complement killing, hemadsorption, and adherence to polystyrene.

Warren L Simmons, Kevin Dybvig

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Current research in microbial sciences · 2022
    Review
  4. A Review ofFrontiers in veterinary science · 2021
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Mycoplasma polysaccharide protects against complement.Microbiology (Reading, England) · 2012
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Mycoplasma biofilms ex vivo and in vivo.FEMS microbiology letters · 2009
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

2 authors at 1 institution in 1 country.

Warren L SimmonsDepartment of Genetics, University of Alabama at Birmingham, 720 South 20th Street, Kaul Room 720, Birmingham, AL 35294, USA. wsimmons@uab.edu
Kevin Dybvig
University of Alabama at Birmingham · US

Funding

GENETIC RECOMBINATION IN MYCOPLASMASR01GM051126 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DYBVIG, KEVIN F · 1997 to 2004
$1.1M
Antigenic Variation in MycoplasmasR21AI041113 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DYBVIG, KEVIN F · 2004 to 2004
$337k
ANTIGENIC VARIATION IN MYCOPLASMASR01AI041113 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DYBVIG, KEVIN F · 1997 to 2000
$200k
GENETIC RECOMBINATION IN MYCOPLASMASR21GM051126 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DYBVIG, KEVIN F · 1995 to 1996
–
NIAID NIH HHS AI 41113NIGMS NIH HHS GM 51126NIGMS NIH HHS R01 GM051126
6 · The paper itself

Abstract

The variable surface antigens (Vsa) of the murine respiratory pathogen Mycoplasma pulmonis are associated with the virulence of the microorganism in the lung. In strain UAB CT, the antigens consist of an N-terminal region that is combined with one of seven different C-terminal variable regions comprised of tandem repeats. M. pulmonis producing a VsaA protein with about 40 tandem repeats (R40) does not adhere to red blood cells or polystyrene. Strains that produce VsaH contain a short C-terminal region that lacks tandem repeats and adhere to red blood cells and plastic. We isolated and analyzed M. pulmonis strain CT variants (CT182 and derivatives) that produced a VsaA protein with only three tandem repeats (R3). These variants adhered to plastic and red blood cells similarly to the VsaH-producing strain. When the R3-producing CT182 strain or the VsaH-producing strains were incubated with normal guinea pig serum, they were efficiently killed. Killing was abolished when the serum was heat inactivated. In contrast, the M. pulmonis strains that produced VsaA R40 were highly resistant to complement killing. CT182R3 variants that survived the complement killing reactions all produced the R40 form of VsaA and were resistant to complement killing. VsaA R40 is the first mycoplasmal protein shown to be associated with resistance to complement. As both VsaH and VsaA can mediate adherence to plastic, cytadherence, and susceptibility to complement, we propose that Vsa modulates these phenotypes by nonspecific interactions.

Indexed as

AnimalsAntigens, BacterialAntigens, SurfaceBacterial AdhesionBacterial ProteinsBase SequenceComplement System ProteinsDNA, BacterialGuinea PigsHemadsorptionHumansIn Vitro TechniquesMycoplasmaMycoplasma InfectionsPolystyrenesTandem Repeat SequencesAntigens, BacterialAntigens, SurfaceBacterial ProteinsComplement System ProteinsDNA, BacterialPolystyrenes

Identifiers

PMID14500494
PMCPMC201092
OpenAlexW2156911999

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.