Neutrophil killing of two type 1 fimbria-bearing Escherichia coli strains: dependence on respiratory burst activation.

The production of reactive oxygen metabolites by neutrophils is thought to play a key role in host defense against invading microorganisms. In this study, the generation of oxygen metabolites induced by two uropathogenic Escherichia coli strains, ABU2 and PN7, and their subsequent killing in neutrophils were investigated. Both strains were grown to promote type 1 (mannose-sensitive) fimbria formation, but they differ with respect to other surface structures. When interacting with human neutrophils, the ABU2 bacteria adhered to and were phagocytized by the neutrophils, whereas PN7 bacteria adhered to the neutrophils but resisted phagocytosis. Both strains induced a pronounced neutrophil chemiluminescence response. However, when the intracellular and extracellular parts of the oxidative response were separated, we found that the predominant part of the response was of intracellular origin with the ABU2 bacteria as prey, whereas a large fraction of the response induced by the PN7 bacteria was extracellular. The general opinion is that production of reactive oxygen metabolites should be intraphagosomal to minimize the tissue-damaging effects of the metabolites and to optimize their bactericidal effects. However, since the surface-adherent bacteria (the PN7 cells) are killed in an aerobic but not an anaerobic milieu, whereas the ingested bacteria (the ABU2 cells) are killed in both aerobic and anaerobic milieu, we propose that extracellularly generated oxygen metabolites are of importance in killing E. coli strains that can resist neutrophil engulfment.