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PLoS One. 2014 Mar 6;9(3):e90960. doi: 10.1371/journal.pone.0090960. eCollection 2014.

Interleukin-15 and soluble interleukin-15 receptor α in coronary artery disease patients: association with epicardial fat and indices of adipose tissue distribution.

Author information

1
Department of Biomedical Sciences for Health, Chair of Clinical Pathology, Università degli Studi di Milano, Milan, Italy.
2
Diabetology and Metabolic Diseases Unit, I.R.C.C.S. Policlinico San Donato, San Donato Milanese, Milan, Italy.
3
Cardiology Unit, I.R.C.C.S. Policlinico San Donato, San Donato Milanese, Milan, Italy.
4
Cardiac Surgery Unit, I.R.C.C.S. Policlinico San Donato, San Donato Milanese, Milan, Italy.
5
Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, Regensburg, Germany.
6
Department of Biomedical Sciences for Health, Chair of Clinical Pathology, Università degli Studi di Milano, Milan, Italy; Service of Laboratory Medicine 1-Clinical Pathology, Department of Health Services of Diagnosis and Treatment-Laboratory Medicine, I.R.C.C.S. Policlinico San Donato, San Donato Milanese, Milan, Italy.

Abstract

Interleukin-15 (IL-15) is a pro-inflammatory cytokine which signals via a specific alpha receptor subunit (IL-15Rα). Increased IL-15 level has been observed in cardiovascular patients and IL-15 immunoreactivity has been detected at vulnerable atherosclerotic plaques. Due to the association between adipose tissue distribution, inflammation and coronary artery disease (CAD), we quantified IL-15 and IL-15Rα in CAD patients with different adiposity and adipose tissue distribution and we evaluated whether epicardial adipose tissue (EAT), a visceral fat depot surrounding and infiltrating myocardium, may be a source of both molecules. IL-15 and IL-15Rα proteins were quantified by enzyme-linked immunosorbent assays. Gene expression of IL-15 and IL-15Rα in EAT depots was evaluated by one colour microarray platform. EAT thickness was measured by echocardiography. Plasmatic IL-15 and IL-15Rα levels were higher in CAD than non-CAD patients. After classification according to adipose tissue distribution, IL-15 was higher in CAD patients with increased abdominal adiposity. Increased level of IL-15Rα was observed both in CAD and non-CAD patients with increased abdominal fat. EAT was a source of IL-15 and IL-15Rα and their expression was higher in CAD patients with increased EAT thickness. In conclusion, our data suggest that circulating levels of IL-15 and IL-15Rα seem to reflect visceral distribution of adipose tissue and that EAT may be a potential source of both IL-15 and IL-15Rα. Future studies on the relationship between IL-15, visceral fat and characteristics of atherosclerotic plaques could help to better understand the complex biology of this cytokine.

PMID:
24603895
PMCID:
PMC3948349
DOI:
10.1371/journal.pone.0090960
[Indexed for MEDLINE]
Free PMC Article
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