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Patients with insulin-dependent diabetes or coronary heart disease following rehabilitation express serum fractalkine levels similar to those in healthy control subjects

The chemokine and adhesion molecule fractalkine and its receptor CX(3)CR1 have emerged as interesting regulators in inflammation and related atherosclerosis. The pro-inflammatory status may be counteracted by appropriate treatment, such as in rehabilitation. We compared serum fractalkine concentrati...

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Autores principales: Maegdefessel, Lars, Schlitt, Axel, Pippig, Susanna, Schwaab, Bernhard, Fingscheidt, Kerstin, Raaz, Uwe, Buerke, Michael, Loppnow, Harald
Formato: Texto
Lenguaje:English
Publicado: Dove Medical Press 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2762434/
https://www.ncbi.nlm.nih.gov/pubmed/19851523
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author Maegdefessel, Lars
Schlitt, Axel
Pippig, Susanna
Schwaab, Bernhard
Fingscheidt, Kerstin
Raaz, Uwe
Buerke, Michael
Loppnow, Harald
author_facet Maegdefessel, Lars
Schlitt, Axel
Pippig, Susanna
Schwaab, Bernhard
Fingscheidt, Kerstin
Raaz, Uwe
Buerke, Michael
Loppnow, Harald
author_sort Maegdefessel, Lars
collection PubMed
description The chemokine and adhesion molecule fractalkine and its receptor CX(3)CR1 have emerged as interesting regulators in inflammation and related atherosclerosis. The pro-inflammatory status may be counteracted by appropriate treatment, such as in rehabilitation. We compared serum fractalkine concentrations of 46 patients with coronary heart disease (CHD) and 47 insulin-dependent diabetic patients (IDDM) following rehabilitation with those of 50 control subjects. Following rehabilitation serum fractalkine levels (477 ± 225 pg/mL) in CHD patients were similar to those in control subjects (572 ± 205 pg/mL; P = 0.303), whereas fractalkine levels were lower in IDDM patients (430 ± 256 pg/mL; P = 0.042). No significant difference between CHD and IDDM patients was present (P = 0.319). Postprandial hyperlipemia may influence inflammation; thus, we investigated fractalkine levels four and eight hours after inducing postprandial hyperlipemia. However, we did not find any significant alterations in CHD and diabetic patients, whereas the fractalkine levels in controls were reduced. In vitro, lipofundin used as a hyperlipemic stimulus was added to vessel wall cells and reduced fractalkine levels. Low fractalkine levels in patients attending rehabilitation indicate a beneficial effect of the rehabilitation procedure on innate inflammatory pathways, such as the chemokine and adhesion molecule fractalkine.
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spelling pubmed-27624342009-10-22 Patients with insulin-dependent diabetes or coronary heart disease following rehabilitation express serum fractalkine levels similar to those in healthy control subjects Maegdefessel, Lars Schlitt, Axel Pippig, Susanna Schwaab, Bernhard Fingscheidt, Kerstin Raaz, Uwe Buerke, Michael Loppnow, Harald Vasc Health Risk Manag Original Research The chemokine and adhesion molecule fractalkine and its receptor CX(3)CR1 have emerged as interesting regulators in inflammation and related atherosclerosis. The pro-inflammatory status may be counteracted by appropriate treatment, such as in rehabilitation. We compared serum fractalkine concentrations of 46 patients with coronary heart disease (CHD) and 47 insulin-dependent diabetic patients (IDDM) following rehabilitation with those of 50 control subjects. Following rehabilitation serum fractalkine levels (477 ± 225 pg/mL) in CHD patients were similar to those in control subjects (572 ± 205 pg/mL; P = 0.303), whereas fractalkine levels were lower in IDDM patients (430 ± 256 pg/mL; P = 0.042). No significant difference between CHD and IDDM patients was present (P = 0.319). Postprandial hyperlipemia may influence inflammation; thus, we investigated fractalkine levels four and eight hours after inducing postprandial hyperlipemia. However, we did not find any significant alterations in CHD and diabetic patients, whereas the fractalkine levels in controls were reduced. In vitro, lipofundin used as a hyperlipemic stimulus was added to vessel wall cells and reduced fractalkine levels. Low fractalkine levels in patients attending rehabilitation indicate a beneficial effect of the rehabilitation procedure on innate inflammatory pathways, such as the chemokine and adhesion molecule fractalkine. Dove Medical Press 2009 2009-10-12 /pmc/articles/PMC2762434/ /pubmed/19851523 Text en © 2009 Maegdefessel et al, publisher and licensee Dove Medical Press Ltd. This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.
spellingShingle Original Research
Maegdefessel, Lars
Schlitt, Axel
Pippig, Susanna
Schwaab, Bernhard
Fingscheidt, Kerstin
Raaz, Uwe
Buerke, Michael
Loppnow, Harald
Patients with insulin-dependent diabetes or coronary heart disease following rehabilitation express serum fractalkine levels similar to those in healthy control subjects
title Patients with insulin-dependent diabetes or coronary heart disease following rehabilitation express serum fractalkine levels similar to those in healthy control subjects
title_full Patients with insulin-dependent diabetes or coronary heart disease following rehabilitation express serum fractalkine levels similar to those in healthy control subjects
title_fullStr Patients with insulin-dependent diabetes or coronary heart disease following rehabilitation express serum fractalkine levels similar to those in healthy control subjects
title_full_unstemmed Patients with insulin-dependent diabetes or coronary heart disease following rehabilitation express serum fractalkine levels similar to those in healthy control subjects
title_short Patients with insulin-dependent diabetes or coronary heart disease following rehabilitation express serum fractalkine levels similar to those in healthy control subjects
title_sort patients with insulin-dependent diabetes or coronary heart disease following rehabilitation express serum fractalkine levels similar to those in healthy control subjects
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2762434/
https://www.ncbi.nlm.nih.gov/pubmed/19851523
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