Vitamin D and macrophage polarization in epicardial adipose tissue of atherosclerotic swine.

Autor: Gunasekar P; Department of Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE, United States of America., Swier VJ; Department of Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE, United States of America., Fleegel JP; Department of Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE, United States of America., Boosani CS; Department of Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE, United States of America., Radwan MM; Department of Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE, United States of America., Agrawal DK; Department of Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE, United States of America.
Jazyk: angličtina
Zdroj: PloS one [PLoS One] 2018 Oct 08; Vol. 13 (10), pp. e0199411. Date of Electronic Publication: 2018 Oct 08 (Print Publication: 2018).
DOI: 10.1371/journal.pone.0199411
Abstrakt: Vitamin D functions as a potent immunomodulator by interacting with many immune cells however, its role in regulating inflammation in the epicardial adipose tissue (EAT) is unclear. In the EAT of atherosclerotic microswine that were fed with deficient, sufficient or supplemented levels of vitamin D, we evaluated the phenotype of the macrophages. Vitamin D treatment was continued for 12 months and serum 25(OH)D levels were measured regularly. Infiltration of M1/M2 macrophage was investigated by immunostaining for CCR7 and CD206, respectively in conjunction with a pan macrophage marker CD14. Significant difference in the number of CCR7+ cells was observed in the EAT from vitamin D-deficient swine compared to vitamin D-sufficient or -supplemented swine. Expression of CD206 correlated with high levels of serum 25(OH)D indicating a significant increase in M2 macrophages in the EAT of vitamin D-supplemented compared to -deficient swine. These findings suggest that vitamin D-deficiency exacerbates inflammation by increasing pro-inflammatory M1 macrophages, while vitamin D-supplementation attenuates the inflammatory cytokines and promotes M2 macrophages in EAT. This study demonstrates the significance of vitamin D mediated inhibition of macrophage mediated inflammation in the EAT during coronary intervention in addition to its immunomodulatory role. However, additional studies are required to identify the cellular mechanisms that transduce signals between macrophages and smooth muscle cells during restenosis in the presence and absence of vitamin D.
Competing Interests: The corresponding author received research grants from the National Institutes of Health, USA, and has no other financial interest or disclosure. The authors have no relevant affiliations or financial involvement with any organization or entity with financial interest or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.
Databáze: MEDLINE
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