title: In vivo extravasated human monocytes have an altered expression of CD16, HLA-DR, CD86, CD36 and CX(3)CR1.
abstract: The phenotypic alterations in monocytes induced by extravasation in vivo are still largely unknown. We addressed the question whether a general phenotype of extravasated monocytes exists and whether this phenotype differs between healthy individuals and statin treated patients with coronary artery disease (CAD). In vivo extravasated monocytes from CAD patients and healthy controls were collected by use of the skin blister method and compared with peripheral circulating monocytes by flow cytometry. The number of CD14(+)CD16(+) monocytes were significantly higher in the skin blister compared with peripheral circulation in both patients (P < 0.001) and controls (P = 0.005). In vivo extravasated monocytes had in comparison with peripheral monocytes a lower expression of CX(3)CR1, a higher expression of HLA-DR, CD86 and CD36 and a higher binding of acetylated low density lipoprotein (acLDL) (significant for all markers). Skin blister fluid from CAD patients, compared with healthy controls, induced a 20% increase in monocyte CD36 expression (P = 0.008) following 18 h of in vitro incubation. The results indicate that the integrated response to the in vivo extravasation process is similar in statin treated stable CAD patients and healthy controls, with respect to phenotypic alterations. Such differences in CAD patients may, however, occur as a response to the inflammatory milieu.
authors.affiliation: Department of Clinical Immunology and Allergy, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden. josefin.paulsson@ki.se
authors.forename: J M
authors.initials: JM
authors.lastname: Paulsson
authors.forename: C
authors.initials: C
authors.lastname: Held
authors.forename: S H
authors.initials: SH
authors.lastname: Jacobson
authors.forename: J
authors.initials: J
authors.lastname: Lundahl
mesh_terms: D000368:Aged; D051940:B7-2 Antigen / Q000378:metabolism*; D001768:Blister / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D018955:CD36 Antigens / Q000378:metabolism*; D000073883:CX3C Chemokine Receptor 1; D002452:Cell Count; D002465:Cell Movement / Q000276:immunology*; D003324:Coronary Artery Disease / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism; D005260:Female; D058851:GPI-Linked Proteins; D006684:HLA-DR Antigens / Q000378:metabolism*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D019707:Receptors, Chemokine / Q000378:metabolism*; D017452:Receptors, IgG / Q000378:metabolism*
chemical_list: D051940:B7-2 Antigen; D018955:CD36 Antigens; C497964:CD86 protein, human; D000073883:CX3C Chemokine Receptor 1; C095235:CX3CR1 protein, human; C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D006684:HLA-DR Antigens; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008077:Lipoproteins, LDL; D019707:Receptors, Chemokine; D017452:Receptors, IgG; C032629:acetyl-LDL