Deacylated lipopolysaccharide inhibits plasminogen activator inhibitor-1, prostacyclin, and prostaglandin E2 induction by lipopolysaccharide but not by tumor necrosis factor-alpha. J Immunol 1990 May 01;144(9):3506-12
Date
05/01/1990Pubmed ID
2109778Scopus ID
2-s2.0-0025232732 (requires institutional sign-in at Scopus site) 46 CitationsAbstract
Bacterial LPS and TNF induce vascular endothelial cells to express a variety of response molecules. LPS that is partially deacylated (dLPS) by a human neutrophil enzyme blocks the ability of LPS, but not TNF, to augment one of these responses, the expression of endothelial cell surface molecules that promote neutrophil adherence (J. Exp. Med. 1987; 165:1393-1402). We show that dLPS can inhibit the ability of LPS, but not TNF, to elicit the expression of plasminogen activator inhibitor-1 (PAI-1), prostacyclin, and PGE2 by human umbilical vein endothelial cells. dLPS also prevented the accumulation of specific PAI-1 mRNA in response to LPS, but not to TNF. Neither the LPS- or TNF-induced expression of PAI-1 nor the dLPS inhibition of the LPS response was mediated by prostanoids. These results indicate that dLPS can specifically block a variety of endothelial cell responses to LPS and provide support for the hypotheses 1) that dLPS and LPS may interact with a common target molecule on or in endothelial cells, and 2) that dLPS, produced by enzymatic deacylation of LPS in vivo, could inhibit endothelial cell stimulation by LPS and thereby limit the host inflammatory response to invasive gram-negative bacteria.
Author List
Riedo FX, Munford RS, Campbell WB, Reisch JS, Chien KR, Gerard RDAuthor
William B. Campbell PhD Professor in the Pharmacology and Toxicology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AcylationBlotting, Northern
Dinoprostone
Dose-Response Relationship, Drug
Endothelium, Vascular
Epoprostenol
Gene Expression
Humans
In Vitro Techniques
Lipopolysaccharides
Plasminogen Inactivators
RNA, Messenger
Structure-Activity Relationship
Tumor Necrosis Factor-alpha
