Diminished neutrophil oxidative metabolism after phagocytosis of virulent Salmonella typhi

Abstract

The interactions of human polymorphonuclear neutrophils (PMNs) with virulent and avirulent strains of Salmonella typhi were examined. Ingestion of the S. typhi strains by PMNs was evaluated with three techniques: visual examination of PMN monolayers (phagocytic index); uptake of radiolabeled S. typhi by PMNs; and removal of S. typhi from the supernatant of suspensions of PMNs and bacteria. All three techniques indicated equivalent phagocytosis of the strains. Postphagocytic PMN oxidative metabolism was quantitated with measurements of oxygen consumption, protein iodination, and chemiluminescence. We found that although PMNs ingested equal numbers of virulent and avirulent S. typhi, those PMNs ingesting the virulent organisms exhibited a significantly smaller increase in postphagocytic oxidative metabolism than PMNs ingesting avirulent S. typhi. Despite this muted oxidative burst the virulent bacteria were killed as well as the avirulent strains. Virulent S. typhi either fail to stimulate receptors that trigger PMN oxidative metabolism or inhibit PMN oxidative metabolism. Our data support the former hypothesis.

Intracellular Salmonella typhimurium Induce Lysis of Human Polymorphonuclear Leukocytes Which Is Not Associated with the Salmonella Virulence Plasmid

“…Ofloxacin treatment only did not produce any significant toxic effect on non-infected PMNs ( and in most cases, the cell lysis was seen accompanying an expansion of the intracellular bacterial number (B). Smears were made 24 hr after infection, stained with Wright stain, and examined by a light microscope at a magnification of 1,000. lent strains, in contrast, are unable to block the respiratory burst but that both virulent and avirulent strains of S. typhi are equally killed in human PMNs (12). Our data showed that PMNs responded well to the stimuli of S. typhimurium, not only to the moderately virulent strains including the plasmidless but also to the fully virulent strain.…”

Helicobacter pylori induces but survives the extracellular release of oxygen radicals from professional phagocytes using its catalase activity

“…Other bacterial pathogens have evolved mechanisms to evade the oxidative response of phagocytes. For example, Toxoplasma gondii (Anderson and Remington, 1974), Yersinia pestis (Chanetzky et al, 1985), Y. enterocolitica (Lian et al, 1987), Brucella abortus (Kreutzer et al, 1979), Salmonella typhi (Kossack et al, 1981), Chlamydia trachomatis (Hammerschlag et al, 1985) and Mycobacterium leprae (Holzer et al, 1986) elicit little or no oxidative burst. In contrast, some adherent N. gonorrhoeae variants induce an enhanced oxidative burst (Knepper et al, 1997), but one that results in little release of oxidative metabolites into the extracellular milieu (Naids and Rest, 1991).…”

Particle‐induced myeloperoxidase release in serially diluted whole blood quantifies the number and the phagocytic activity of blood neutrophils and opsonization capacity of plasma

“…Because phagocytosing leukocytes constitute the first line of the body's defence mechanism against invading microbial pathogens, CL-related studies of RB-activity have been used to assess the influence of various pathophysiological states of the host on the antimicrobial activity of granulocytes (10,(12)(13)(14)(15)(16)(17)(18)(19)(20)(21). These studies have been performed mainly by using isolated leukocytes.…”