Evidence map›Paper›PMID 27376197›Full record

ArticleBiosensors & bioelectronics2016

Impact of CCL2 and CCR2 chemokine/receptor deficiencies on macrophage recruitment and continuous glucose monitoring in vivo.

Ulrike Klueh, Caroline Czajkowski, Izabela Ludzinska, Yi Qiao, Jackman Frailey, Donald L Kreutzer

Open access · greenAbstract read
In one paragraph

Article in Biosensors & bioelectronics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  15. Macrophage function in obesity-induced inflammation and insulin resistance.Pflugers Archiv : European journal of physiology · 2017
    Review
  16. Article
  17. Review
  18. Obesity: An Immunometabolic Perspective.Frontiers in endocrinology · 2016
    Review
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

6 authors at 1 institution in 1 country.

Ulrike KluehCenter for Molecular Tissue Engineering, University of Connecticut, School of Medicine, Farmington, CT 06030, USA; Department of Surgery, University of Connecticut, School of Medicine, Farmington, CT 06030, USA. Electronic address: klueh@uchc.edu.
Caroline CzajkowskiCenter for Molecular Tissue Engineering, University of Connecticut, School of Medicine, Farmington, CT 06030, USA; Department of Surgery, University of Connecticut, School of Medicine, Farmington, CT 06030, USA.
Izabela LudzinskaCenter for Molecular Tissue Engineering, University of Connecticut, School of Medicine, Farmington, CT 06030, USA; Department of Surgery, University of Connecticut, School of Medicine, Farmington, CT 06030, USA.
Yi QiaoCenter for Molecular Tissue Engineering, University of Connecticut, School of Medicine, Farmington, CT 06030, USA; Department of Surgery, University of Connecticut, School of Medicine, Farmington, CT 06030, USA.
Jackman FraileyCenter for Molecular Tissue Engineering, University of Connecticut, School of Medicine, Farmington, CT 06030, USA; Department of Surgery, University of Connecticut, School of Medicine, Farmington, CT 06030, USA.
Donald L KreutzerCenter for Molecular Tissue Engineering, University of Connecticut, School of Medicine, Farmington, CT 06030, USA; Department of Surgery, University of Connecticut, School of Medicine, Farmington, CT 06030, USA.
University of Connecticut · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAVID P OLSON · 2013 to 2026
$24.3M
Macrophages and Biosensor Function in VivoR01DK081171 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI KREUTZER, DON · 2009 to 2013
$2.3M
Impact of the Vascular System and CGMDP3DK101082 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI KREUTZER, DON · 2013 to 2013
$1.8M
NIDDK NIH HHS DP3 DK101082NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK081171
6 · The paper itself

Abstract

The accumulation of macrophages (MΦ) at the sensor-tissue interface is thought to be a major player in controlling tissue reactions and sensor performance in vivo. Nevertheless until recently no direct demonstration of the causal relationship between MΦ aggregation and loss of sensor function existed. Using a Continuous Glucose Monitoring (CGM) murine model we previously demonstrated that genetic deficiencies of MΦ or depletion of MΦ decreased MΦ accumulation at sensor implantation sites, which led to significantly enhanced CGM performance, when compared to normal mice. Additional studies in our laboratories have also demonstrated that MΦ can act as "metabolic sinks" by depleting glucose levels at the implanted sensors in vitro and in vivo. In the present study we extended these observations by demonstrating that MΦ chemokine (CCL2) and receptor (CCR2) knockout mice displayed a decrease in inflammation and MΦ recruitment at sensor implantation sites, when compared to normal mice. This decreased MΦ recruitment significantly enhanced CGM performance when compared to control mice. These studies demonstrated the importance of the CCL2 family of chemokines and related receptors in MΦ recruitment and sensor performance and suggest chemokine targets for enhancing CGM in vivo.

Indexed as

AnimalsBlood GlucoseBlood Glucose Self-MonitoringCells, CulturedChemokine CCL2MacrophagesMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMonitoring, AmbulatoryReceptors, CCR2Reproducibility of ResultsSensitivity and SpecificityBlood GlucoseCcl2 protein, mouseCcr2 protein, mouseChemokine CCL2Receptors, CCR2ChemotaxisContinuous glucose monitoringDiabetesInflammationMacrophage

Identifiers

PMID27376197
PMCPMC5028269
OpenAlexW2462845232

What Socratic 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 Socratic graph.