Activated endothelial cells limit inflammatory response, but increase chemoattractant potential and bacterial clearance by XXXX monocytes.

@entity1 @entity650 @entity5750 @entity4222 @entity1356 @entity310 @entity3963 @entity3962 @entity2842 @entity4071 @entity2939 @entity687 @entity1366
UNASSIGNED: Inflammation is the normal immune response of vascularized tissues to damage and bacterial products, for which leukocyte @entity4222 ( @entity4222 ) is critical. The effects of cell-to-cell contact seen in both leukocyte and endothelial cells include cytoskeleton rearrangement, and dynamic expression of adhesion molecules and metalloproteinases. @entity4222 induces expression of anti-apoptotic molecules, costimulatory molecules associated with antigen presentation, and pattern recognition receptors (PRR), such as @entity2939 , in monocytes. However, little is known about how @entity2939 increment operates in monocytes during an inflammatory response. To understand it better, we used an in vitro model in which monocytes crossed a layer of @entity1356 stimulated @entity1 Umbilical Vein Endothelial Cells (HUVEC). After @entity4222 , monocytes were tested for the secretion of inflammatory cytokines and chemokines, their phenotype ( @entity5750 , @entity4071 , @entity2939 expression), and @entity2939 canonical [Nuclear Factor kappa B, (NF-kB) pathway] and non-canonical [ @entity3963 , @entity3962 pathway] signal transduction induced by lipopolysaccharide (LPS). Phagocytosis and bacterial clearance were also measured. There was diminished secretion of LPS-induced inflammatory cytokines ( @entity1356 , @entity650 , and @entity310 ) and higher secretion of chemokines ( @entity687 / @entity687 and @entity2842 / @entity2842 ) in supernatant of @entity4222 monocytes. These changes were accompanied by increases in @entity2939 , @entity5750 (surfaces expression), @entity3963 , and @entity1366 phosphorylated cytoplasmic forms, without affecting NF-kB activation. It also increased bacterial clearance after @entity4222 by an O2 -independent mechanism. The data suggest that interaction between endothelial cells and monocytes fine-tunes the inflammatory response and promotes bacterial elimination.
