title: Monocyte subtypes predict clinical course and prognosis in human stroke.
abstract: The number of circulating monocytes increases after stroke. In this study, we assessed the time course and phenotype of monocyte subsets and their relationship with the clinical course and outcome in 46 consecutive stroke patients and 13 age-matched controls. The proportion of the most abundant 'classical' CD14(high)CD16- monocytes did not change after stroke, whereas that of CD14(high)CD16+ monocytes increased and CD14(dim)CD16+ monocytes decreased. CD14(high)CD16+ monocytes had the highest expression of TLR2, HLA-DR and the angiogenic marker, Tie-2; CD14(dim)CD16+ monocytes had the highest expression of costimulatory CD86 and adhesion molecule CD49d. Platelet-monocyte interactions were highest in CD14(high)CD16- monocytes and lowest in CD14(dim)CD16+ monocytes. In adjusted models, 1/CD14(high)CD16- monocytes were associated with poor outcome (OR: 1.38), higher mortality (OR: 1.40) and early clinical worsening (OR: 1.29); 2/CD14(high)CD16+ monocytes were inversely related to mortality (OR: 0.32); and 3/CD14(dim)CD16+ monocytes were inversely related to poor outcome (OR: 0.74) and infarction size (r=-0.45; P=0.02). These results illustrate that the predominant monocyte subtype conveys harmful effects after stroke, which include stronger interaction with platelets. Alternatively, rarer subpopulations of monocytes are beneficial with a phenotype that could promote tissue repair and angiogenesis. Therefore, monitoring of monocyte subtypes may emerge as a useful tool at the bedside for stroke patients.
authors.affiliation: Functional Unit of Cerebrovascular Diseases, Hospital Clínic, Barcelona, Spain.
authors.forename: Xabier
authors.initials: X
authors.lastname: Urra
authors.forename: Neus
authors.initials: N
authors.lastname: Villamor
authors.forename: Sergio
authors.initials: S
authors.lastname: Amaro
authors.forename: Manuel
authors.initials: M
authors.lastname: Gómez-Choco
authors.forename: Víctor
authors.initials: V
authors.lastname: Obach
authors.forename: Laura
authors.initials: L
authors.lastname: Oleaga
authors.forename: Anna M
authors.initials: AM
authors.lastname: Planas
authors.forename: Angel
authors.initials: A
authors.lastname: Chamorro
mesh_terms: D000368:Aged; D001792:Blood Platelets / Q000166:cytology / Q000276:immunology; D016022:Case-Control Studies; D005260:Female; D058851:GPI-Linked Proteins; D006801:Humans; D007958:Leukocyte Count; D018950:Lipopolysaccharide Receptors / Q000096:biosynthesis*; D016015:Logistic Models; D008297:Male; D009000:Monocytes / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D018919:Neovascularization, Physiologic / Q000276:immunology; D010641:Phenotype; D011237:Predictive Value of Tests; D011379:Prognosis; D017452:Receptors, IgG / Q000096:biosynthesis*; D020521:Stroke / Q000097:blood / Q000276:immunology* / Q000401:mortality / Q000503:physiopathology; D013997:Time Factors
chemical_list: C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D018950:Lipopolysaccharide Receptors; D017452:Receptors, IgG