Either CD14 ++CD16 + or CD14 ++CD16 − monocytes can independently predict future cardiovascular events and the outcome after myocardial infarction 8, 9, 10, 11. Various clinical studies in patients with coronary artery disease (CAD) or myocardial infarction have evaluated monocyte subsets. Cluster analysis has revealed that this intermediate subset closely relates to CD16 − monocytes and resembles proinflammatroy murine Ly6C hi/Gr-1 + rather than Ly6C low/Gr-1 − monocytes 4, 6, 7. This subset, however, has gained interest as it can secrete high amounts of TNF-α in response to LPS stimulation 5. More recent work has identified an additional intermediate monocyte subset: CD14 ++CD16 + monocytes numerically represent the smallest monocyte population. CD14 ++CD16 − monocytes, frequently described as classical monocytes, dominate in the peripheral circulation, compared to ‘non-classical’ CD14 +CD16 ++. In humans, monocyte subsets differ in their expressions of the LPS receptor CD14 and the FcγIII receptor CD16. Their subsets, defined by surface markers both in mice and humans, show distinct and divergent functions and play specialized roles in the formation and propagation of atherosclerotic lesions 2, 4. Monocytes display considerable heterogeneity. Beyond their role in initial lesion formation, monocytes also participate in the progression of atherosclerotic lesions, and the precipitation of thrombotic complications 3. Local accumulation of leukocytes helps drive atherosclerotic lesion formation, and during the last decade monocytes have gained growing attention as key contributors to atherogenesis 2. A deeper understanding of its cellular and molecular mechanisms could aid the development of tailored therapies for atherosclerosis and its complications.

Despite improvement in the interventional and pharmacological treatment of atherosclerosis, this disease remains a leading cause of death in developed countries. These data suggest substantial dynamics in monocyte subset distributions and phenotypes in different stages of PAOD, which can either serve as biomarkers or as potential therapeutic targets to decrease the inflammatory burden in advanced stages of atherosclerosis.Ītherosclerosis, a chronic inflammatory disease of the arterial wall, remains the underlying cause of cardiovascular complications such as myocardial infarction, stroke, and peripheral artery occlusive disease (PAOD) 1. Likewise, increased CD162 and MPO expression was noted in CD14 ++CD16 − classical monocytes. Moreover, CD162 and MPO expression increased significantly in intermediate monocyte subsets in advanced disease stages. Proportions of CD14 ++CD16 + intermediate monocyte levels were significantly increased in advanced stages of PAOD, while classical and non-classical monocytes displayed no such trend. Additionally the expression of distinct surface markers (CD106, CD162 and myeloperoxidase MPO) was analyzed. Peripheral blood was obtained from 143 patients suffering from PAOD (Rutherford stage I to VI) and three monocyte subsets were identified by flow cytometry: CD14 ++CD16 − classical monocytes, CD14 +CD16 ++ non-classical monocytes and CD14 ++CD16 + intermediate monocytes. Therefore, we aimed to investigate monocyte subset heterogeneity in patients with PAOD. While the role of monocyte subset heterogeneity has already been well investigated in coronary artery disease (CAD), the knowledge about monocytes and their heterogeneity in peripheral artery occlusive disease (PAOD) still is limited. Human monocytes display a considerable heterogeneity and at least three subsets can be distinguished. Monocytes are key players in atherosclerotic.

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