title: Monocyte-platelet complexes on CD14/CD16 monocyte subsets: relationship with ApoA-I levels. A preliminary study.
abstract: The adhesion of the monocytes to the endothelium and their extravasation into the intima are key steps in atherogenesis. Studies showed the essential role of L-selectin (CD62-L), expressed by the monocytes, and the platelets by forming complexes with monocytes. The delipided apolipoprotein (Apo) A or high-density lipoprotein (HDL) has antiinflammatory effects on monocytes and can bind platelets (monocyte-platelet complexes [MPCs]). The aim of this study was to identify a possible relationship between the MPCs, the monocyte subset, and ApoA-I/HDL serum levels in vivo. Platelet-monocyte complexes were estimated by flow cytometry in 16 volunteers. Monocyte-platelet interaction was characterized by the percentage of monocytes coexpressing the constitutive platelet marker, glycocalicin gpIb-alpha (CD42b; CD42b+monocytes in %, MPC%). Monocytes were divided into four subsets based on lipopolysaccharide receptor (CD14) and FcgammaIII receptor (CD16) expression (CD14++/CD16-, G1; CD14++/CD16+, G2; CD14+/CD16-, G3; and CD14+/CD16+, G4). HDL and ApoA-I levels were measured by routine laboratory techniques. MPC% in the different subsets were G1=8.1+/-3.4%, G2=21.2+/-14%, G3=18+/-12.6%, and G4=22.3+/-14.3% (analysis of variance: P<.001). MPC% in the entire monocyte population was negatively correlated to ApoA-I (R=-0.71, P=.001). The relationship between ApoA-I and MPC% was found mainly in the subsets G1 (R=-0.67, P=.001) and G2 (R=-0.61, P=.01). MPC% was not correlated with any other lipids or lipoprotein or high-sensitivity C-reactive protein. When whole blood was incubated with HDL/ApoA-I, no modification of platelet CD42b fluorescence was observed, indicating that there is no direct interaction between the HDL/ApoA-I and the CD42b fluorescence. Among the monocytes, the G2 subset appeared to have the highest extravasation potential. Indeed, we previously showed that those cells overexpressed CD62-L, and we observed in this work that they were coated with platelets more than the G1 cells. The G2 subset could be more directly involved in the development of atherosclerotic lesions.
authors.affiliation: Laboratoire de Médecine Expérimentale (ULB 222 Unit), ISPPC Hopital André Vesale, Montigny-Le-Tilleul, Belgium. karim.zouaoui@chu-charleroi.be
authors.forename: Karim Zouaoui
authors.initials: KZ
authors.lastname: Boudjeltia
authors.forename: Dany
authors.initials: D
authors.lastname: Brohee
authors.forename: Pietrina
authors.initials: P
authors.lastname: Piro
authors.forename: Vincent
authors.initials: V
authors.lastname: Nuyens
authors.forename: Jean
authors.initials: J
authors.lastname: Ducobu
authors.forename: Myriam
authors.initials: M
authors.lastname: Kherkofs
authors.forename: Pierre
authors.initials: P
authors.lastname: Van Antwerpen
authors.forename: Philippe
authors.initials: P
authors.lastname: Cauchie
authors.forename: Claude
authors.initials: C
authors.lastname: Remacle
authors.forename: Michael
authors.initials: M
authors.lastname: Vanhaeverbeek
mesh_terms: D000328:Adult; D016632:Apolipoprotein A-I / Q000097:blood*; D001792:Blood Platelets / Q000166:cytology* / Q000378:metabolism; D005434:Flow Cytometry; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000096:biosynthesis*; D009000:Monocytes / Q000166:cytology* / Q000378:metabolism; D017452:Receptors, IgG / Q000096:biosynthesis*
chemical_list: D016632:Apolipoprotein A-I; D018950:Lipopolysaccharide Receptors; D017452:Receptors, IgG