Evidence map›Paper›PMID 21525381›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Staphylococcus aureus biofilms prevent macrophage phagocytosis and attenuate inflammation in vivo.

Lance R Thurlow, Mark L Hanke, Teresa Fritz, Amanda Angle, Amy Aldrich, Stetson H Williams, Ian L Engebretsen, Kenneth W Bayles, Alexander R Horswill, Tammy Kielian

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 392 papers.

0numbers the graph read from it
0cells of the map it votes in
392citing papers in PubMed
13.6field-weighted citation impact, top 1% 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

392 citing papers in PubMed, 682 citations in OpenAlex.

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332 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

10 authors at 3 institutions in 1 country.

Lance R ThurlowDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Mark L Hanke
Teresa Fritz
Amanda Angle
Amy Aldrich
Stetson H Williams
Ian L Engebretsen
Kenneth W Bayles
Alexander R Horswill
Tammy Kielian
University of Nebraska Medical Center · USUniversity of Iowa · USWayne State College · US

Funding

The S. aureus biofilm lifecycleP01AI083211 · NIAID · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAYLES, KENNETH W. · 2009 to 2023
$32.1M
The molecular control of bacterial autolysisR01AI038901 · NIAID · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAYLES, KENNETH W. · 2003 to 2012
$3.1M
NIAID NIH HHS P01 AI083211NIAID NIH HHS R01 AI038901
6 · The paper itself

Abstract

Biofilms are complex communities of bacteria encased in a matrix composed primarily of polysaccharides, extracellular DNA, and protein. Staphylococcus aureus can form biofilm infections, which are often debilitating due to their chronicity and recalcitrance to antibiotic therapy. Currently, the immune mechanisms elicited during biofilm growth and their impact on bacterial clearance remain to be defined. We used a mouse model of catheter-associated biofilm infection to assess the functional importance of TLR2 and TLR9 in the host immune response during biofilm formation, because ligands for both receptors are present within the biofilm. Interestingly, neither TLR2 nor TLR9 impacted bacterial density or inflammatory mediator secretion during biofilm growth in vivo, suggesting that S. aureus biofilms circumvent these traditional bacterial recognition pathways. Several potential mechanisms were identified to account for biofilm evasion of innate immunity, including significant reductions in IL-1β, TNF-α, CXCL2, and CCL2 expression during biofilm infection compared with the wound healing response elicited by sterile catheters, limited macrophage invasion into biofilms in vivo, and a skewing of the immune response away from a microbicidal phenotype as evidenced by decreases in inducible NO synthase expression concomitant with robust arginase-1 induction. Coculture studies of macrophages with S. aureus biofilms in vitro revealed that macrophages successful at biofilm invasion displayed limited phagocytosis and gene expression patterns reminiscent of alternatively activated M2 macrophages. Collectively, these findings demonstrate that S. aureus biofilms are capable of attenuating traditional host proinflammatory responses, which may explain why biofilm infections persist in an immunocompetent host.

Indexed as

BiofilmsAnimalsCatheter-Related InfectionsCytokinesGreen Fluorescent ProteinsHost-Pathogen InteractionsImmune EvasionInflammationMacrophagesMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroscopy, ConfocalMicroscopy, Electron, ScanningModels, ImmunologicalCytokinesGreen Fluorescent ProteinsTlr2 protein, mouseTlr9 protein, mouseToll-Like Receptor 2Toll-Like Receptor 9

Identifiers

PMID21525381
PMCPMC3110737
OpenAlexW1907075739

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.