Evidence map›Paper›PMID 22025727›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Polymorphisms in fibronectin binding protein A of Staphylococcus aureus are associated with infection of cardiovascular devices.

Steven K Lower, Supaporn Lamlertthon, Nadia N Casillas-Ituarte, Roberto D Lins, Ruchirej Yongsunthon, Eric S Taylor, Alex C DiBartola, Catherine Edmonson, Lauren M McIntyre, L Barth Reller and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

47 citing papers in PubMed, 74 citations in OpenAlex.

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  9. Frontiers in cellular and infection microbiology · 2022
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  16. Surface Proteins ofMicrobiology spectrum · 2019
    Review
  17. Article
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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

14 authors at 7 institutions in 4 countries.

Steven K LowerOhio State University, Columbus, OH 43210, USA. lower.9@osu.edu
Supaporn Lamlertthon
Nadia N Casillas-Ituarte
Roberto D Lins
Ruchirej Yongsunthon
Eric S Taylor
Alex C DiBartola
Catherine Edmonson
Lauren M McIntyre
L Barth Reller
Yok-Ai Que
Robert Ros
Brian H Lower
Vance G Fowler
The Ohio State University · USDuke University Hospital · USUniversity of Florida · USArizona State University · USDuke Medical Center · USUniversidade Federal de Pernambuco · BRUniversity of Lausanne · CH

Funding

Host Susceptibility to S. aureusR01AI068804 · NIAID · DUKE UNIVERSITY · PI FOWLER, VANCE G. · 2007 to 2016
$6.9M
Mentoring Patient Oriented Research in Antibiotic-Resistant BacteriaK24AI093969 · NIAID · DUKE UNIVERSITY · PI FOWLER, VANCE G. · 2011 to 2020
$1.6M
Forces at the heart of Staphylococcus biofilms on cardiac implantsR21HL086593 · NHLBI · OHIO STATE UNIVERSITY · PI LOWER, STEVEN K · 2008 to 2009
$430k
NHLBI NIH HHS R21 HL086593NHLBI NIH HHS R21HL086593NIAID NIH HHS K24 AI093969NIAID NIH HHS K24AI093969NIAID NIH HHS R01 AI068804NIAID NIH HHS R01AI068804
6 · The paper itself

Abstract

Medical implants, like cardiovascular devices, improve the quality of life for countless individuals but may become infected with bacteria like Staphylococcus aureus. Such infections take the form of a biofilm, a structured community of bacterial cells adherent to the surface of a solid substrate. Every biofilm begins with an attractive force or bond between bacterium and substratum. We used atomic force microscopy to probe experimentally forces between a fibronectin-coated surface (i.e., proxy for an implanted cardiac device) and fibronectin-binding receptors on the surface of individual living bacteria from each of 80 clinical isolates of S. aureus. These isolates originated from humans with infected cardiac devices (CDI; n = 26), uninfected cardiac devices (n = 20), and the anterior nares of asymptomatic subjects (n = 34). CDI isolates exhibited a distinct binding-force signature and had specific single amino acid polymorphisms in fibronectin-binding protein A corresponding to E652D, H782Q, and K786N. In silico molecular dynamics simulations demonstrate that residues D652, Q782, and N786 in fibronectin-binding protein A form extra hydrogen bonds with fibronectin, complementing the higher binding force and energy measured by atomic force microscopy for the CDI isolates. This study is significant, because it links pathogenic bacteria biofilms from the length scale of bonds acting across a nanometer-scale space to the clinical presentation of disease at the human dimension.

Indexed as

Polymorphism, GeneticAdhesins, BacterialAmino Acid SequenceAmino Acid SubstitutionBiofilmsHumansMicroscopy, Atomic ForceMolecular Dynamics SimulationMolecular Sequence DataPacemaker, ArtificialSequence Homology, Amino AcidStaphylococcus aureusAdhesins, Bacterialfibronectin-binding proteins, bacterial

Identifiers

PMID22025727
PMCPMC3215016
OpenAlexW2096228560

What OpenQuestion holds

Textmetadata
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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.