Soluble @entity7636 in serum mediates LPS-induced increase in permeability of XXXX pulmonary arterial endothelial cell monolayers in vitro.

@entity3126 @entity7636 @entity326 @entity649 @entity291 @entity71840
Lipopolysaccharide (LPS) is a mediator of @entity326 and @entity649 ( @entity649 ), conditions which are characterized by high-permeability @entity3126 . LPS increases endothelial permeability both directly and indirectly via the pro-inflammatory cytokines produced by monocytes and macrophages. We investigated the role of soluble @entity7636 in serum in the increased endothelial permeability induced by LPS. @entity291 pulmonary artery endothelial cells were grown to confluence on a microporous filter and the 125I-albumin clearance rate across the monolayer was determined. Even a high concentration of LPS (1 microgram/ml) did not increase endothelial permeability under a serum-free condition. In the presence of more than 3% normal human serum, LPS increased endothelial permeability. The presence of neutralizing anti- @entity7636 monoclonal antibody eliminated the serum-dependent effect of LPS. The addition of recombinant sCD14 completely replaced the requirement for serum. @entity71840 ( @entity71840 ) did not enhance the rsCD14-mediated LPS effect, and anti- @entity71840 antibody did not attenuate the serum-dependent LPS effect. These findings suggest that sCD14 in serum mediates the permeability-increasing effect on LPS on endothelial cells but that @entity71840 is not necessary for this effect.
