[Inflammation in the perivascular adipose tissue and atherosclerosis].

In atherosclerosis studies, there are few data, especially in men, on the biology of perivascular adipose tissue (PVAT) compared to that of other adipose tissue (AT), on amendments in obesity, and its possible role in the development of atherosclerosis. We conducted an ex vivo human study on pericarotid adipose tissue-collected in the immediate vicinity (PVATp) and away from the plate (tapas)-and subcutaneous (SC) neck gathered during surgery from patients suffering from atheromatous carotid disease. In addition, we conducted a study in obese Zucker rats (models of obesity and insulin resistance) and Wistar rats subjected to moderate stress. In these models, we collected renal adipose tissue (RAT), epididymal adipose tissue (EAT), and TAPA samples. On all samples, we measured mRNA levels encoding for proinflammatory cytokines (TNFα, IL-6, IL-1β, MCP-1). Our results showed an increase in mRNA MCP-1, TNF and IL-6 in the adipose tissue around atherosclerotic plaques, an increase that was greater in diabetics than in non-diabetic subjects; we noted for the mRNA of MCP-1 in the TAPAp, 3.49×10 ^-2 ±1.17×10 ^-2 ng/ug 18S in diabetic patients compared to 7.26×10 ^-3 ±1.00×10 ^-3 ng/ug 18S ( ^** P<0.01) in non-diabetic patients. In the obese Zucker rat, we found a significant increase in IL-6 in TAPA in obese animals compared to the corresponding controls (4.24×10 ^-5 ±1.75×10 ^-6 ng/μg 18S vs 1.29×10 ^-5 ±1.55×10 ^-6 ng/ug 18S). In stressed rats, we recorded a TNFα mRNA increase in the PVAT and EAT in the stressed rats compared to fatty tissue of control animals, we note respectively, 7.52×10 ^-3 ±2.8×10 ^-3 ng/μg 18S vs 2.62×10 ^-3 ±0.57×10 ^-3 ng/18S and 4.78×10 ^-3 ±1.52×10 ^-3 ng/μg 18S vs 2.02×10 ^-3 ±0.3×10 ^-3 ng/ug 18S. In summary, our work shows an inflammatory state of the TAPA surrounding the atheromatous plaques in diabetic patients. An obesity or stress state promotes an inflammatory profile of PVAT.
(Copyright © 2017 Académie des sciences. Published by Elsevier Masson SAS. All rights reserved.)