Abstract
Monocytes are a heterogeneous cell population distinguished into three subsets with distinctive phenotypic and functional properties: “classical” (CD14++CD16-), “intermediate” (CD14++CD16+), and “nonclassical” (CD14+CD16++). Monocyte subsets play a pivotal role in many inflammatory systemic diseases including atherosclerosis (ATS). Only a low number of studies evaluated monocyte behavior in patients affected by cardiovascular diseases, and data about their role in acute aortic dissection (AAD) are lacking. Thus, the aim of this study was to investigate CD14++CD16-, CD14++CD16+, and CD14+CD16++ cells in patients with Stanford-A AAD and in patients with carotid artery stenosis (CAS). Methods. 20 patients with carotid artery stenosis (CAS group), 17 patients with Stanford-A AAD (AAD group), and 17 subjects with traditional cardiovascular risk factors (RF group) were enrolled. Monocyte subset frequency was determined by flow cytometry. Results. Classical monocytes were significantly increased in the AAD group versus CAS and RF groups, whereas intermediate monocytes were significantly decreased in the AAD group versus CAS and RF groups. Conclusions. Results of this study identify in AAD patients a peculiar monocyte array that can partly explain depletion of T CD4+ lymphocyte subpopulations observed in patients affected by AAD.
Highlights
Atherosclerosis (ATS) is a multifactorial disease [1] characterized by an inflammatory remodeling of the arterial wall
Immune response strongly affects the outcome of intraparietal inflammation: T helper (Th) 1 lymphocytes have been mainly associated with plaque formation and Th2 lymphocytes with abdominal aortic aneurism (AAA), whereas macrophages have been related to acute aortic dissection (AAD) [1, 5, 6]
Classical monocytes were significantly increased in the AAD group versus carotid artery stenosis (CAS) and RF groups (p = 0 0342 and p = 0 0422, respectively), whereas intermediate monocytes were significantly decreased in the AAD group versus CAS and RF groups (p = 0 0494 and p = 0 0211, respectively)
Summary
Atherosclerosis (ATS) is a multifactorial disease [1] characterized by an inflammatory remodeling of the arterial wall. Depending on size and site of vessels involved, ATS leads to a wide range of cardiovascular diseases (CVDs) [2], including ischemic heart disease, cerebrovascular disease, carotid artery stenosis (CAS), abdominal aortic aneurism (AAA), acute aortic dissection (AAD), and other conditions [3, 4]. Immune response strongly affects the outcome of intraparietal inflammation: T helper (Th) 1 lymphocytes have been mainly associated with plaque formation and Th2 lymphocytes with AAA, whereas macrophages have been related to AAD [1, 5, 6]. Each monocyte subset possesses distinctive phenotypic and functional properties and displays different immune functions, distinguished by cytokine profiles and phagocytic activity [11]. To our knowledge, data about the role of monocyte subsets in AAD are still lacking
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