Human Monocytes - CD14, CD16 - Ziegler-Heitbrock

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Atrial fibrillation is associated with high levels of monocyte-platelet-aggregates and increased CD11b expression in patients with aortic stenosis.

Abstract

A growing body of evidence suggests a pivotal role of inflammatory processes in AF in a bidirectional manner. Infiltrating leukocytes seem to promote both structural and electrical remodelling processes in patients with AF. Monocyte-platelets-aggregates (MPAs) are sensitive markers of both platelets and monocyte activation. So far it is not clear whether the content of MPAs is affected by AF. The present study examined the content of MPAs and the activation of monocytes in elderly patients with an aortic stenosis in dependence of AF. These patients are known to have a high prevalence of AF. Flow-cytometric quantification analysis demonstrated that patients with AF have an increased content of MPAs (207 ± 13 cells/µl vs 307 ± 21 cells/µl, p< 0.001), and enhanced expression of CD11b on monocytes (p< 0.001), compared to patients in stable sinus rhythm (SR). The number of CD14+/CD16+ monocytes were only slightly elevated in patients with AF. These findings were seen in patients with permanent AF. But also patients with paroxysmal AF, even when presenting in SR, the MPAs were increased by 50 % (p< 0.05) as well as the CD11b expression, which was twice as high (p< 0.05) compared to stable SR. These results demonstrate for the first time a dependency of MPAs and CD11b expression on monocytes in the presence of AF and support the notion of a close relationship between AF, thrombogenesis and inflammation. The content of MPAs and the extent of activation on monocytes appear promising as biomarkers for paroxysmal AF and as possible future targets for developing novel pharmacological therapeutic strategies.

Authors: Pfluecke C, Berndt K, Wydra S, Tarnowski D, Barthel P, Quick S, Ulbrich S, Christoph M, Waessnig N, Speiser U, Wunderlich C, Poitz DM, Strasser RH, Ibrahim K.
Journal: Thromb Haemost.;115(5):993-1000
Year: 2016
PubMed: Find in PubMed