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 Blood, 15 March 2007, Vol. 109, No. 6, pp. 2438-2445.
Prepublished online as a Blood First Edition Paper on November 28, 2006; DOI 10.1182/blood-2006-06-026997.

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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY

Involvement of the fractalkine pathway in the pathogenesis of childhood hemolytic uremic syndrome

María Victoria Ramos1, Gabriela C. Fernández1, Natasha Patey4, Pablo Schierloh1, Ramón Exeni2, Irene Grimoldi2, Graciela Vallejo3, Christian Elías-Costa3, Maria del Carmen Sasiain1, Howard Trachtman7, Christophe Combadière6, François Proulx5, and Marina S. Palermo1

1 Division of Immunology, Institute of Hematological Investigations, Academia Nacional de Medicina, Buenos Aires, Argentina; 2 Department of Nephrology, Hospital Municipal del Niño, San Justo, Argentina; 3 Department of Nephrology, Hospital de Niños "Ricardo Gutiérrez," Buenos Aires, Argentina; 4 Department of Pediatrics, Division of Pediatric Pathology, Hôpital Necker Enfants-Malades, Paris, France; 5 Department of Pediatrics, Division of Pediatric Intensive Care, Ste-Justine Hospital, Montreal, QC, Canada; 6 INSERM (Institut National de la Santé et de la Recherche Médicale) U543, Université Pierre et Marie Curie, Hôpital Pitié-Salpétrière, Paris, France; 7 Department of Pediatrics, Division of Pediatric Nephrology, Schneider Children's Hospital, New York, NY

Thrombotic microangiopathy and acute renal failure are cardinal features of postdiarrheal hemolytic uremic syndrome (HUS). These conditions are related to endothelial and epithelial cell damage induced by Shiga toxin (Stx) through the interaction with its globotriaosyl ceramide receptor. However, inflammatory processes contribute to the pathogenesis of HUS by sensitizing cells to Stx fractalkine (FKN), a CX3C transmembrane chemokine expressed on epithelial and endothelial cells upon activation, is involved in the selective migration and adhesion of specific leukocyte subsets to tissues. Here, we demonstrated a selective depletion of circulating mononuclear leukocytes expressing the receptor for FKN (CX3CR1) in patients with HUS. We found a unique phenotype in children with HUS distinct from that seen in healthy, uremic, or infected controls, in which monocytes lost CX3CR1, down-modulated CD62L, and increased CD16. In addition, the CD56dim natural killer (NK) subpopulation was decreased, leading to an altered peripheral CD56dim/CD56bright ratio from 10.0 to 4.5. It is noteworthy that a negative correlation existed between the percentage of circulating CX3CR1+ leukocytes and the severity of renal failure. Finally, CX3CR1+ leukocytes were observed in renal biopsies from patients with HUS. We suggest that the interaction of CX3CR1+ cells with FKN present on activated endothelial cells may contribute to renal injury in HUS.


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