Profil cytologique des leucémies aigu?s à Casablanca

The diagnosis of AML is based on the clinical and biological arguments. The purpose of this study is to describe cytological characteristics of 814 cases of acute leukemia collected at the Laboratory of Haematology, University Hospital Ibn-Rochd of Casablanca between 1^st January 2004 and 31 July 2007. Morphological examination of bone marrow and the reaction to myeloperoxidase were used to classify acute leukemias: 1) 64% of acute leukemias are the myeloid type (AML); 2) 30% of acute leukemias are the lymphoblastic type (ALL); 3) 6% of acute leukemias are difficult to classify according to criteria of the FAB group. In this series, 81.6% of AML cases are seen in adults with a sex ratio M/F of 1.05, for ALL, 67.3% of cases are diagnosed in children with a sex ratio M/F of 1.2. According to FAB classification, and the LAM1 and LAM2 are most frequent, respectively 31% and 28 %, for lymphoblastic form, type 2 is predominant with 75%.     

Platelet-derived sphingosine-1-phosphate and inflammation: from basic mechanisms to clinical implications

Beyond key functions in hemostasis and thrombosis, platelets are recognized as key players of inflammation, an underlying feature of a variety of diseases. In this regard, platelets act as a circulating source of several pro- and anti-inflammatory molecules, which are secreted from their intracellular stores upon activation. Among them, mounting evidence highlights a crucial role of sphingosine-1-phosphate (S1P), a multifunctional sphingoid mediator. S1P-induced pleiotropic effects include those crucial in inflammatory processes, such as the maintenance of the endothelial barrier integrity, and leukocyte activation and recruitment at the injured site. This review outlines the peculiar features and molecular mechanisms that allow platelets for acting as a unique factory that produces and stores S1P in large quantities. A particular emphasis is placed on the autocrine and paracrine roles of S1P derived from the “inflamed” platelets, highlighting the role of its cross-talk with endothelial and blood cells involved in inflammation, and the mechanisms of its contribution to the development and progression of inflammatory diseases. Finally, potential clinical implications of platelet-derived S1P as diagnostic tool of inflammatory severity, and as therapeutic target in inflammation are discussed.     

The surface protein HvgA mediates group B streptococcus hypervirulence and meningeal tropism in neonates

Streptococcus agalactiae (group B streptococcus; GBS) is a normal constituent of the intestinal microflora and the major cause of human neonatal meningitis. A single clone, GBS ST-17, is strongly associated with a deadly form of the infection called late-onset disease (LOD), which is characterized by meningitis in infants after the first week of life. The pathophysiology of LOD remains poorly understood, but our epidemiological and histopathological results point to an oral route of infection. Here, we identify a novel ST-17-specific surface-anchored protein that we call hypervirulent GBS adhesin (HvgA), and demonstrate that its expression is required for GBS hypervirulence. GBS strains that express HvgA adhered more efficiently to intestinal epithelial cells, choroid plexus epithelial cells, and microvascular endothelial cells that constitute the blood-brain barrier (BBB), than did strains that do not express HvgA. Heterologous expression of HvgA in nonadhesive bacteria conferred the ability to adhere to intestinal barrier and BBB-constituting cells. In orally inoculated mice, HvgA was required for intestinal colonization and translocation across the intestinal barrier and the BBB, leading to meningitis. In conclusion, HvgA is a critical virulence trait of GBS in the neonatal context and stands as a promising target for the development of novel diagnostic and antibacterial strategies.