Increased serum levels of fractalkine and mobilisation of CD34+CD45− endothelial progenitor cells in systemic sclerosis

Autor: Audrey Benyamine, Elisabeth Jouve, Françoise Dignat-George, Philippe Berbis, Gilles Kaplanski, Pascale Paul, Jeremy Magalon, Yves Frances, Sylvie Cointe, Nathalie Bardin, Jean-Robert Harlé, Romaric Lacroix, Laurent Arnaud, F. Bernard-Guervilly, Pascal Rossi, Brigitte Granel, Pierre-Jean Weiller, Nathalie Lesavre, David Braunstein, Françoise Couranjou, Florence Sabatier
Přispěvatelé: Vascular research center of Marseille (VRCM), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire Géomatériaux (DGCB-LGM), École Nationale des Travaux Publics de l'État (ENTPE)-Centre National de la Recherche Scientifique (CNRS), Service de Médecine Interne, Centre Hospitalier Universitaire de Saint-Etienne [CHU Saint-Etienne] (CHU ST-E), Service de Chirurgie, Assistance Publique - Hôpitaux de Marseille (APHM)-Hospices Civiles de Marseille-Hôpital de la Conception [CHU - APHM] (LA CONCEPTION), Hôpital de la Timone [CHU - APHM] (TIMONE), Hôpital Nord [CHU - APHM], Physiopathologie du stress pancréatique, Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Aix Marseille Université (AMU), Hôpital nord
Jazyk: angličtina
Rok vydání: 2017
Předmět:
Zdroj: Arthritis Research and Therapy
Arthritis Research and Therapy, 2017, 19 (1), ⟨10.1186/s13075-017-1271-7⟩
Arthritis Research and Therapy, BioMed Central, 2017, 19 (1), ⟨10.1186/s13075-017-1271-7⟩
ISSN: 1478-6354
DOI: 10.1186/s13075-017-1271-7⟩
Popis: The disruption of endothelial homeostasis is a major determinant in the pathogenesis of systemic sclerosis (SSc) and is reflected by soluble and cellular markers of activation, injury and repair. We aimed to provide a combined assessment of endothelial markers to delineate specific profiles associated with SSc disease and its severity. We conducted an observational, single-centre study comprising 45 patients with SSc and 41 healthy control subjects. Flow cytometry was used to quantify circulating endothelial microparticles (EMPs) and CD34+ progenitor cell subsets. Colony-forming unit-endothelial cells (CFU-ECs) were counted by culture assay. Circulating endothelial cells were enumerated using anti-CD146-based immunomagnetic separation. Blood levels of endothelin-1, vascular endothelial growth factor (VEGF) and soluble fractalkine (s-Fractalkine) were evaluated by enzyme-linked immunosorbent assay. Disease-associated markers were identified using univariate, correlation and multivariate analyses. Enhanced numbers of EMPs, CFU-ECs and non-haematopoietic CD34+CD45− endothelial progenitor cells (EPCs) were observed in patients with SSc. Patients with SSc also displayed higher serum levels of VEGF, endothelin-1 and s-Fractalkine. s-Fractalkine levels positively correlated with CD34+CD45− EPC numbers. EMPs, s-Fractalkine and endothelin-1 were independent factors associated with SSc. Patients with high CD34+CD45− EPC numbers had lower forced vital capacity values. Elevated s-Fractalkine levels were associated with disease severity, a higher frequency of pulmonary fibrosis and altered carbon monoxide diffusion. This study identifies the mobilisation of CD34+CD45− EPCs and high levels of s-Fractalkine as specific features of SSc-associated vascular activation and disease severity. This signature may provide novel insights linking endothelial inflammation and defective repair processes in the pathogenesis of SSc.
Databáze: OpenAIRE
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