Erschienen in:
01.12.2012 | Original Contribution
Pro-inflammatory effects of the mushroom Agaricus blazei and its consequences on atherosclerosis development
verfasst von:
Juliana L. Gonçalves, Eric H. Roma, Ana Cristina Gomes-Santos, Edenil C. Aguilar, Daniel Cisalpino, Luciana R. Fernandes, Angélica T. Vieira, Dirce R. Oliveira, Valbert N. Cardoso, Mauro M. Teixeira, Jacqueline I. Alvarez-Leite
Erschienen in:
European Journal of Nutrition
|
Ausgabe 8/2012
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Abstract
Purpose
Extracts of the mushroom Agaricus blazei (A.
blazei) have been described as possessing immunomodulatory and potentially cancer-protective activities. However, these effects of A.
blazei as a functional food have not been fully investigated in vivo.
Methods
Using apolipoprotein E-deficient (ApoE−/−) mice, an experimental model of atherosclerosis, we evaluated the effects of 6 or 12 weeks of A.
blazei supplementation on the activation of immune cells in the spleen and blood and on the development of atherosclerosis.
Results
Food intake, weight gain, blood lipid profile, and glycemia were similar between the groups. To evaluate leukocyte homing and activation, mice were injected with 99mTc-radiolabeled leukocytes, which showed enhanced leukocyte migration to the spleen and heart of A. blazei-supplemented animals. Analysis of the spleen showed higher levels of activation of neutrophils, NKT cells, and monocytes as well as increased production of TNF-α and IFN-γ. Circulating NKT cells and monocytes were also more activated in the supplemented group. Atherosclerotic lesion areas were larger in the aorta of supplemented mice and exhibited increased numbers of macrophages and neutrophils and a thinner fibrous cap. A. blazei-induced transcriptional upregulation of molecules linked to macrophage activation (CD36, TLR4), neutrophil chemotaxy (CXCL1), leukocyte adhesion (VCAM-1), and plaque vulnerability (MMP9) were seen after 12 weeks of supplementation.
Conclusions
This is the first in vivo study showing that the immunostimulatory effect of A. blazei has proatherogenic repercussions. A. blazei enhances local and systemic inflammation, upregulating pro-inflammatory molecules, and enhancing leukocyte homing to atherosclerosis sites without affecting the lipoprotein profile.