Evidence map›Paper›PMID 23365077›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Targeting macrophage activation for the prevention and treatment of Staphylococcus aureus biofilm infections.

Mark L Hanke, Cortney E Heim, Amanda Angle, Sam D Sanderson, Tammy Kielian

Erratum issued Registry-linked trialAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT03271580 (Biofilm Modified Macrophage Phenotype and Function in Diabetic Wound Healing), which is not on this map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
–field-weighted citation impact
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.

NCT03271580 terminatednot on this mapstarted 2020, after this paper: background citation

Biofilm Modified Macrophage Phenotype and Function in Diabetic Wound Healing

TypeobservationalSponsorIndiana UniversityRan2020 to 2021Enrolled31ConditionsWound, Bacterial Infections, Diabetes Mellitus, Infected Ulcer of SkinArmsFinger prick test for HbA1c measurement, Punch Biopsy, Vac Sponge Collection, Ankle Brachial Index
3 · Its place in the literature

Who cites it

90 citing papers in PubMed.

  1. Review
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  3. Article
  4. Article
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  10. Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Matrix porosity is associated withbioRxiv : the preprint server for biology · 2024
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

30 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

5 authors.

Mark L HankeDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Cortney E Heim
Amanda Angle
Sam D Sanderson
Tammy Kielian

Funding

The S. aureus biofilm lifecycleP01AI083211 · NIAID · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAYLES, KENNETH W. · 2009 to 2023
$32.1M
NIAID NIH HHS P01 AI083211
6 · The paper itself

Abstract

Biofilm infections often lead to significant morbidity due to their chronicity and recalcitrance to antibiotics. We have demonstrated that methicillin-resistant Staphylococcus aureus (MRSA) biofilms can evade macrophage (MΦ) antibacterial effector mechanisms by skewing MΦs toward an alternatively activated M2 phenotype. To overcome this immune evasion, we have used two complementary approaches. In the first, a proinflammatory milieu was elicited by local administration of classically activated M1 MΦs and in the second by treatment with the C5a receptor (CD88) agonist EP67, which invokes MΦ proinflammatory activity. Early administration of M1-activated MΦs or EP67 significantly attenuated biofilm formation in a mouse model of MRSA catheter-associated infection. Several proinflammatory mediators were significantly elevated in biofilm-infected tissues from MΦ- and EP67-treated animals, revealing effective reprogramming of the biofilm environment to a proinflammatory milieu. A requirement for MΦ proinflammatory activity was demonstrated by the fact that transfer of MyD88-deficient MΦs had minimal impact on biofilm growth. Likewise, neutrophil administration had no effect on biofilm formation. Treatment of established biofilm infections with M1-activated MΦs also significantly reduced catheter-associated biofilm burdens compared with antibiotic treatment. Collectively, these results demonstrate that targeting MΦ proinflammatory activity can overcome the local immune inhibitory environment created during biofilm infections and represents a novel therapeutic strategy.

Indexed as

AnimalsBiofilmsCatheter-Related InfectionsCells, CulturedHumansImmune EvasionInflammationMacrophage ActivationMacrophagesMethicillin-Resistant Staphylococcus aureusMiceMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88NeutrophilsOligopeptidesMyd88 protein, mouseMyeloid Differentiation Factor 88OligopeptidesReceptor, Anaphylatoxin C5atyrosyl-seryl-phenylalanyl-lysyl-aspartyl-methionyl-prolyl-N-methyleucyl-alanyl-arginine

Identifiers

PMID23365077
PMCPMC3578052

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.