Sensitivity of K1-Encapsulated Escherichia coli to Killing by the Bactericidal/Permeability-Increasing Protein of Rabbit and Human Neutrophils

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Abstract
The presence of K1 capsular polysaccharides increases the resistance of E. coli to killing by serum and phagocytosis by polymorphonuclear leukocytes (PMN). To determine whether K1 capsule impedes the action of intracellular bactericidal and non-encapsulated strains of E. coli to killing by the bactericidal/permeability-increasing protein (BPI) isolated from rabbit and human PMN was compared. BPI appears to be the principal bactericidal agent of PMN toward E. coli and other gram-negative bacteria. The presence of K1 capsule was monitored by sensitivity to K1-specific bacteriophages. The non-encapsulated strains used represent both random bacteremic isolates and non-encapsulated derivatives of K1-encapsulated strains obtained by selection for resistance to K1-specific phages. Little or no difference was found in the sensitivity of K1-encapsulated and non-encapsulated E. coli to killing by neutralized acid extracts of rabbit PMN. Bacterial killing by these crude fractions can be attributed to the action of BPI because: bacterial killing was blocked by immune (anti-BPI) Ig but not by preimmune Ig and comparison of the dose-response curves of bacterial killing by crude extracts and by purified BPI showed that the bactericidal activity of crude extracts and by purified BPI showed that the bactericidal activity of crude fractions corresponded closely to the BPI content. Human and rabbit BPI exhibited similar bactericidal potency toward K1-encapsulated E. coli; i.e., < 5 .mu.g of either protein killed > 90% of 2.5 .times. 107 bacteria. Thus, the potent bactericidal action of BPI toward E. coli is not impeded by K1 capsule, suggesting that the virulence of K1-encapsulated E. coli is a consequence of extracellular survival but not of resistance to intracellular killing.