Abstract:

The role played by bacterial lipopolysaccharides (endotoxins) (LPS) in the initiation of tissue damage during bacterial infections, is well established. It is accepted that LPS is released from the invading bacteria following autolysis, and the interaction of the solubilized LPS with tissues and body fluids lead to the initiation of the physiological, pharmacological and pathological sequelae seen after infections with Gram negative bacterial. Previous studies from our laboratories have shown that the binding of LPS to membranes of RBC is markedly enhanced by heat-labile leukocyte factors2, and that leukocyte factors are also capable of activating ‘LPS’ for binding to cell surfaces. Since the ‘activation’ of LPS caused by this factor \s inhibited by protease inhibitors, it was postulated that proteases present Hn leukocytes and in inflammatory exudates may enhance tissue damage by increasing the passive sensitization of mammalian cells by LPS to subsequent lysis in the presence of antibodies and complement.