TY - JOUR
TI - Effects of Adiponectin in TNF-alpha, IL-6, and IL-10 Cytokine Production
from Coronary Artery Disease Macrophages
AU - Kyriazi, E.
AU - Tsiotra, P. C.
AU - Boutati, E.
AU - Ikonomidis, I. and
AU - Fountoulaki, K.
AU - Maratou, E.
AU - Lekakis, J.
AU - Dimitriadis, G. and
AU - Kremastinos, D. T.
AU - Raptis, S. A.
JO - Hormone and Metabolic Research
PY - 2011
VL - 43
TODO - 8
SP - 537-544
PB - Georg Thieme Verlag KG
SN - 0018-5043, 1439-4286
TODO - 10.1055/s-0031-1277227
TODO - proinflammatory cytokines; atherosclerosis; adiponectin; macrophages
TODO - Adiponectin, an adipose tissue secreted protein, exhibits
anti-inflammatory and antiatherogenic properties. We examined the
effects of the globular and full-length adiponectin on cytokine
production in macrophages derived from Coronary Artery Disease (CAD)
patients and control individuals. Adiponectin’s effects in human
macrophages upon lipopolysaccharide (LPS) treatment were also examined.
Full length adiponectin acted differently on TNF-alpha and IL-6
production by upregulating TNF-alpha and IL-6 protein production, but
not their mRNA expression. Additionally, full length adiponectin was
unable to abrogate LPS proinflammatory effect in TNF-alpha and IL-6 mRNA
expression in CAD and NON-CAD macrophages. In contrast, globular
adiponectin appeared to have proinflammatory properties by potently
upregulating TNF-a and IL-6 mRNA and protein secretion in human
macrophages while subsequently rendered cells resistant to further
proinflammatory stimuli. Moreover, both forms of adiponectin powerfully
suppressed scavenger MSR-AI mRNA expression and augmented IL-10 protein
release, both occurring independently of the presence of LPS or CAD.
These data indicate that adiponectin could potentially protect human
macrophages via the elevated IL-10 secretion and the suppression of
MSR-AI expression. It can also be protective in CAD patients since the
reduced adiponectin-induced IL-6 release in CAD macrophages compared to
controls, could be beneficial in the development of inflammation related
atherosclerosis.
ER -