Endotoxin in vitro interactions with human neutrophils: depression of chemiluminescence, oxygen consumption, superoxide production, and killing

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Abstract
[Escherichia coli] endotoxin [etox] depressed neutrophil bactericidal activity while enhancing nitro blue tetrazolium reduction and hexose monophosphate shunt activity. Separation of bactericidal action from oxidative metabolism suggests that the toxic effect of etox may involve the formation of reactive oxygen radicals such as O2-. Chemiluminescence often accompanies metabolic activation of polymorphonuclear neutrophils (PMN). Human PMN did not show chemiluminescence when challenged with etox (lipopolysaccharide; LPS) or [Salmonella] lipid A. O2- formation was unaffected by etox. Pre-incubation of PMN with LPS for 30 min produced significant depression of chemiluminescence, O2 consumption and O2- formation. Decreased chemiluminescence was not the result of complement consumption. In a cell-free system, superoxide was not scavenged by LPS nor did LPS stimulate superoxide dismutase. Oxidase enzymes for NADH or NADPH harvested from broken cells were not affected by LPS. The toxicity of LPS may reside in its ability to activate the PMN while simultaneously blocking bactericidal capacity.