Differential effects of bacterial lipopolysaccharides upon neutrophil function

• Published in: FEBS letters 1998-07, Vol.430 (3), p.363-369
• Main Authors: Ruchaud-Sparagano, Marie-Hélène, Ruivenkamp, Claudia A, Riches, Philip L, Poxton, Ian R, Dransfield, Ian
• Format: Article
• Language: English
• Subjects: ACLB, albumin-coated latex beads; CD18 Antigens - blood; CD18 Antigens - metabolism; Cell Adhesion - drug effects; Cell Size - drug effects; Endotoxin; fMLP, formyl-Met-Leu-Phe; Humans; Inflammation; LBP, lipopolysaccharide binding protein; Lipopolysaccharides - chemistry; Lipopolysaccharides - pharmacology; LPS, lipopolysaccharide; Macrophage-1 Antigen - blood; Molecular Weight; N-Formylmethionine Leucyl-Phenylalanine - pharmacology; Neutrophil; Neutrophils - cytology; Neutrophils - drug effects; Neutrophils - metabolism; PAF, platelet activating factor; Reactive Oxygen Species; Respiratory Burst - drug effects; Superoxides - blood; TNF, tumour necrosis factor
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/S0014-5793(98)00686-3

Lipopolysaccharide (LPS) is a potent inflammatory agent which augments neutrophil sensitivity to subsequent inflammatory stimuli. In this study, the effects of structurally different LPS types upon neutrophil effector functions were examined. Rough LPS types, which have lost the O-polysaccharide moiety, were found to act more rapidly than smooth LPS types in stimulating neutrophil β 2 integrin activity and fMLP-induced respiratory burst. These findings suggest an involvement of the O-polysaccharide region of LPS in regulating neutrophil responsiveness to different LPS chemotypes with important implications for the mechanisms underlying regulation of the inflammatory response in conditions associated with elevation of LPS in plasma, e.g. septic shock or acute respiratory distress syndrome.