1887

Abstract

We have used salicylhydroxamic acid (SHAM) to inhibit intraphagosomal myeloperoxidase activity in order to evaluate the role of this enzyme in the killing of by human neutrophils. 50 µ-SHAM reduced the luminol-dependent chemiluminescence response stimulated during phagocytosis of unopsonized latex beads and opsonized by over 80% and 60%, respectively. When opsonized were incubated with neutrophils, 45% were killed within 15 min incubation and 60% by 1 h. However, in neutrophil suspensions incubated with 50 µ-SHAM, only 13% were killed by 15 min whilst 71% still remained viable after 1 h. This inhibitor had no effect upon the number of bacteria phagocytosed or upon degranulation. In a cell-free system, 2·5 µ-HO alone killed 55% of the bacteria, whereas in the presence of myeloperoxidase (i.e. 10 mU myeloperoxidase and 2·5 µ-HO) virtually all of the bacteria were killed: the addition of 50 µ-SHAM abolished this myeloperoxidase-enhanced killing but did not affect the HO-dependent killing. We therefore conclude that in normal neutrophils whilst HO is required for killing of this pathogen, both myeloperoxidase-dependent and -independent pathways exist.

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/content/journal/micro/10.1099/00221287-135-5-1187
1989-05-01
2019-11-12
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http://instance.metastore.ingenta.com/content/journal/micro/10.1099/00221287-135-5-1187
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