title: Haemodialysis monocytopenia: differential sequestration kinetics of CD14+CD16+ and CD14++ blood monocyte subsets.
abstract: In peripheral blood the majority of circulating monocytes present a CD14highCD16- (CD14++) phenotype, while a subpopulation shows a CD14lowCD16+ (CD14+CD16+) surface expression. During haemodialysis (HD) using cellulosic membranes transient leukopenia occurs. In contrast, synthetic biocompatible membranes do not induce this effect. We compared the sequestration kinetics for the CD14+CD16+ and CD14++ monocyte subsets during haemodialysis using biocompatible dialysers. Significant monocytopenia, as measured by the leucocyte count, occurred only during the first 30 min. However, remarkable differences were observed between the different monocyte subsets. CD14++ monocyte numbers dropped to 77 +/- 13% of the predialysis level after 15 min, increasing to > or = 93% after 60 min. In contrast, the CD14+CD16+ subset decreased to 33 +/- 15% at 30 min and remained suppressed for the course of dialysis (67 +/- 11% at 240 min). Approximately 6 h after the end of HD the CD14+CD16+ cells returned to basal levels. Interestingly, the CD14+CD16+ monocytes did not show rebound monocytosis while a slight monocytosis of CD14++ monocytes was occasionally observed during HD. A decline in CD11c surface density paralleled the sequestration of CD14+CD16+ monocytes. Basal surface densities of important adhesion receptors differed significantly between the CD14+CD16+ and CD14++ subsets. In conclusion, during HD the CD14+CD16+ subset revealed different sequestration kinetics, with a more pronounced and longer disappearance from the blood circulation, compared with CD14++ monocytes. This sequestration kinetics may be due to a distinct surface expression of major adhesion receptors which facilitate leucocyte-leucocyte, as well as leucocyte-endothelial, interactions.
authors.affiliation: Institute of Clinical Chemistry, Hospital München-Bogenhausen and 2nd Medical Department, Hospital München-Harlaching, München, Germany.
authors.forename: W A
authors.initials: WA
authors.lastname: Nockher
authors.forename: J
authors.initials: J
authors.lastname: Wiemer
authors.forename: J E
authors.initials: JE
authors.lastname: Scherberich
mesh_terms: D018821:CD18 Antigens / Q000096:biosynthesis / Q000097:blood; D002450:Cell Communication / Q000276:immunology; D002465:Cell Movement / Q000276:immunology; D006098:Granulocytes / Q000473:pathology; D006801:Humans; D016130:Immunophenotyping; D016167:Integrin alphaXbeta2 / Q000096:biosynthesis / Q000097:blood; D007700:Kinetics; D007958:Leukocyte Count; D007964:Leukocytosis / Q000097:blood / Q000276:immunology; D007970:Leukopenia / Q000097:blood / Q000276:immunology*; D018950:Lipopolysaccharide Receptors / Q000096:biosynthesis* / Q000097:blood; D009000:Monocytes / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000096:biosynthesis / Q000097:blood; D017452:Receptors, IgG / Q000096:biosynthesis* / Q000097:blood; D016028:Receptors, Leukocyte-Adhesion / Q000096:biosynthesis / Q000097:blood; D006435:Renal Dialysis / Q000009:adverse effects
chemical_list: D018821:CD18 Antigens; D016167:Integrin alphaXbeta2; D018950:Lipopolysaccharide Receptors; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D017452:Receptors, IgG; D016028:Receptors, Leukocyte-Adhesion