Abstract
Both Brucella abortus lipopolysaccharide (LPS) and lipid A were low activators of nitroblue tetrazolium reduction and lysozyme release in human neutrophils. The stimulation was dose dependent and was higher in the presence of autologous plasma than in its absence. The comparison between Brucella LPS and lipid A versus Salmonella LPS revealed that at least 100 times more LPS and 1,000 times more lipid A of the former genus were required to induce significant nitroblue tetrazolium reduction and a corresponding lysozyme release in neutrophils. Low Brucella LPS-mediated superoxide and lysozyme production might contribute to the survival of these facultative intracellular bacteria in phagocytic cells.
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