Beschreibung:
<jats:title>ABSTRACT</jats:title>
<jats:p>
<jats:italic>Neisseria gonorrhoeae</jats:italic>
causes severe exudative urethritis. The exudates from infected individuals contain large numbers of polymorphonuclear leukocytes (PMN) with ingested gonococci. The fate of
<jats:italic>N. gonorrhoeae</jats:italic>
within PMN has been a topic of debate for years. In this study, we examined the interactions of
<jats:italic>N. gonorrhoeae</jats:italic>
with PMN adherent to surfaces as a system that better models events during clinical disease. Using chemiluminescence to measure reactive oxygen species (ROS), we found that
<jats:italic>N. gonorrhoeae</jats:italic>
stimulated PMN to produce a respiratory burst. Different kinetics were seen when PMN were stimulated with opsonized zymosan particles. In addition, ROS were produced predominantly inside the PMN in response to gonococci. Laser scanning confocal microscopy and transmission electron microscopy showed that
<jats:italic>N. gonorrhoeae</jats:italic>
rapidly associated with PMN under these experimental conditions and was internalized. Some gonococci were cleared in the first 30 to 60 min after phagocytosis, but a majority of the population persisted for 6 h after phagocytosis. Quantification of viable organisms showed that a significant portion of the population resisted killing. The viability of this subpopulation remained unchanged for 2 h after phagocytosis. A significant increase of viable gonococci from 1 to 6 h was also observed, suggesting intracellular replication. Four different
<jats:italic>N. gonorrhoeae</jats:italic>
strains demonstrated the same capacity to resist PMN-mediated killing, whereas
<jats:italic>Escherichia coli</jats:italic>
was rapidly killed by PMN under the same conditions. Taken together, these findings suggest that a subpopulation of
<jats:italic>N. gonorrhoeae</jats:italic>
resists killing and replicates within PMN phagosomes in spite of NADPH oxidase activation.
</jats:p>