Neisseria gonorrhoeae survive intraleukocytic oxygen-independent antimicrobial capacities of anaerobic and aerobic granulocytes in the presence of pyocin lethal for extracellular gonococci.
AUTOR(ES)
Casey, S G
RESUMO
The resistance of a piliated, transparent variant of Neisseria gonorrhoeae FA19 to intraleukocytic killing by human polymorphonuclear neutrophils (PMN) was examined. In both aerobic and anaerobic PMN monolayers, approximately 2% of the intracellular gonococci survived for as long as 165 min. Anaerobic PMN were as effective as aerobic PMN in the intracellular killing of gonococci. Hence, O2-independent antimicrobial systems of PMN performed a significant role in the intraleukocytic killing of gonococci were intracellular was supported by the elimination of extracellular bacteria by the addition of pyocin 103 and confirmed by the fluorescent antibody staining of intact gonococci after the PMN were permeabilized to antibody with a Formalin-acetone treatment of PMN monolayers. Our data indicate that while the majority of ingested gonococci are killed by O2-independent antimicrobial systems, a small number (about 2%), survive even when care is taken to eliminate extracellular bacteria.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=261010Documentos Relacionados
- Oxygen-independent intracellular and oxygen-dependent extracellular killing of Escherichia coli S15 by human polymorphonuclear leukocytes.
- Gonococci with mutations to low-level penicillin resistance exhibit increased sensitivity to the oxygen-independent bactericidal activity of human polymorphonuclear leukocyte granule extracts.
- Oxygen-independent killing of Bacteroides fragilis by granule extracts from human polymorphonuclear leukocytes.
- Cloning and characterization of the Escherichia coli hemN gene encoding the oxygen-independent coproporphyrinogen III oxidase.
- Inhibition of Chlamydia psittaci in oxidatively active thioglycolate-elicited macrophages: distinction between lymphokine-mediated oxygen-dependent and oxygen-independent macrophage activation.