PROINFLAMMATORY EFFECTS OF BACTERIAL LIPOPROTEIN ON HUMAN NEUTROPHIL ACTIVATION STATUS, FUNCTION AND CYTOTOXIC POTENTIAL IN VITRO
Autor: | Q D Wu, Jiang Huai Wang, C. Power, S. Sookhai, Henry Paul Redmond |
---|---|
Rok vydání: | 2001 |
Předmět: |
Umbilical Veins
Lipopolysaccharide Neutrophils Phagocytosis Intercellular Adhesion Molecule-1 Macrophage-1 Antigen In Vitro Techniques Critical Care and Intensive Care Medicine Neutrophil Activation Microbiology Proinflammatory cytokine chemistry.chemical_compound Antigens CD Superoxides Intensive care Gram-Negative Bacteria E-selectin Humans Cells Cultured Respiratory Burst Inflammation biology Respiratory burst Chemotaxis Leukocyte chemistry CD18 Antigens Emergency Medicine biology.protein Human umbilical vein endothelial cell Endothelium Vascular E-Selectin Bacterial Outer Membrane Proteins |
Zdroj: | Shock. 15:461-466 |
ISSN: | 1073-2322 |
Popis: | Bacterial lipoprotein (BLP) is the most abundant protein in gram-negative bacterial cell walls, heavily outweighing lipopolysaccharide (LPS). Herein we present findings demonstrating the potent in vitro effects of BLP on neutrophil (PMN) activation status, function, and capacity to transmigrate an endothelial monolayer. PMNs are the principal effectors of the initial host response to injury or infection and constitute a significant threat to invading bacterial pathogens. The systemic inflammatory response syndrome (SIRS) is characterised by significant host tissue injury mediated, in part, by uncontrolled regulation of PMN cytotoxic activity. We found that BLP-activated human PMN as evidenced by increased CD11b/CD18 (Mac-1) expression. Up-regulation of PMN Mac-1 in response to BLP occurred independently of membrane-bound CD14 (mCD14). A similar up-regulation of intercellular adhesion molecule-1 (ICAM-1) on endothelial cells was observed whilst E-Selectin expression was unaffected. PMN transmigration across a human umbilical vein endothelial cell (HUVEC) monolayer was markedly increased after treating either PMN's or HUVEC independently with BLP. This increased transmigration did not occur as a result of any direct effect of BLP on HUVEC monolayer permeability, assessed objectively using the passage of FITC-labeled Dextran-70. BLP primed PMN for enhanced respiratory burst and superoxide anion production in response to PMA, but did not influence phagocytosis of opsonized Escherichia coli. BLP far exceeds LPS as a gram-negative bacterial wall component, these findings therefore implicate BLP as an additional putative mediator of SIRS arising from gram-negative infection. |
Databáze: | OpenAIRE |
Externí odkaz: |