Alginic acid was purified from a mucoid clinical isolate of Pseudomonas aeruginosa. Luminol-dependent chemiluminescence of phorbol myristate acetate-stimulated neutrophils was inhibited by this alginate, but oxygen consumption was unaffected. Further studies indicated that this effect was due to the ability of the pseudomonal alginate to scavenge hypochlorite. A seaweed alginate was less effective and dextran T500 was ineffective in hypochlorite scavenging. It appears that the uronic acid core and the O-acetyl groups of pseudomonal alginate are involved in its hypochlorite-scavenging ability. The relevance of this phenomenon was demonstrated by the greater resistance to killing by hypochlorite of mucoid P. aeruginosa compared with a nonmucoid revertant, and the addition of purified alginate to the nonmucoid revertant protected the organism from hypochlorite. Thus, this extracellular polysaccharide may enhance the virulence of P. aeruginosa by scavenging the phagocyte-generated oxidant HOCI. This enhanced virulence may be involved in disease processes in which mucoid organisms predominate, such as cystic fibrosis.
Previous studies have demonstrated that human eosinophils have a more active hexose monophosphate shunt than neutrophils. However, measurements of superoxide anion production have been variable. In this study human eosinophils are shown to produce one and a half times as much superoxide as neutrophils during a 2-h incubation. The rates of production differed only after the first 30 min of incubation. The production was inhibited by superoxide dismutase in a dose-responsive manner.
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