@entity1446 -Mediated Induction of XXXX and Depletion of CD34+ Progenitor Cells Is @entity2939 Dependent.

@entity1 @entity455 @entity2939 @entity75 @entity409 @entity3964 @entity311 @entity371 @entity204 @entity1446
UNASSIGNED: @entity3964 infection can cause @entity409 , cerebral @entity75 and @entity204 if untreated. We have previously shown that high concentrations of free @entity1446 , and C-X-C motif chemokine 10 ( @entity371 ) in sera of @entity311 @entity1 induce apoptosis in microvascular endothelial and neuronal cells contributing to @entity455 , blood-brain barrier (BBB) damage and mortality. Endothelial progenitor cells (EPC) are microvascular endothelial cell precursors partly responsible for repair and regeneration of damaged BBB endothelium. Studies have shown that EPC's are depleted in severe @entity311 @entity1 , but the mechanisms mediating this phenomenon are unknown. Toll-like receptors recognize a wide variety of pathogen-associated molecular patterns generated by pathogens such as bacteria and parasites. We tested the hypothesis that EPC depletion during @entity311 pathogenesis is a function of @entity1446 -induced apoptosis mediated by @entity371 induction and toll-like receptor (TLR) activation. @entity1446 and @entity371 concentrations in plasma obtained from @entity311 @entity1 were elevated compared with non- @entity311 subjects. EPC numbers were significantly decreased in @entity311 @entity1 (P < 0.02) and @entity2939 expression was significantly elevated in vivo. These findings were confirmed in EPC precursors in vitro; where it was determined that @entity1446 -induced apoptosis and @entity371 expression was @entity2939 -mediated. We conclude that increased serum @entity1446 mediates depletion of EPC during @entity311 pathogenesis.
