Effect of Group B Streptococcal Type-Specific Antigen on Polymorphonuclear Leukocyte Function and Polymorphonuclear Leukocyte- Endothelial Cell Interaction

Abstract

Neonatal group B streptococcal pneumonia is a severe disease, often resulting in death. Autopsy findings resemble those of hyaline membrane disease. Numerous organisms may be seen in the alveoli, but few polymorphonuclear leukocytes (PMNs) are found in the areas of bacterial invasion. Aggregated PMNs are often found, however, in the pulmonary capillaries. This study was designed to explore the effect of the group B streptococcal (GBS) type III antigen on PMN chemotaxis and PMNendothelial cell interactions. Human PMNs were isolated and pretreated with 0.25 to 4 μg/ml of GBS type III antigen prior to determining their chemotactic response to the chemoattractants formyl-methionyl-leucyl-phenylalanine, zymosan-activated serum, platelet-activating factor, and leukotriene B₄. The GBS antigen caused a concentrationdependent inhibition of formyl-methionyl-leucyl-phenylalanine, zymosan-activated serum, and platelet-activating factor-mediated chemotaxis (% inhibition of 38.1 ± 4.0, 55.5 ± 3.3, 46.7 ± 9.7%, respectively; p < 0.01). Leukotriene B₄-mediated chemotaxis was not significantly depressed (21.2% ± 7.7 inhibition; NSD). Group B streptococcal antigen also inhibited formyl-methionyl-Ieucylphenylalanine- induced PMN adherence to endothelial cells in a concentration-dependent fashion when incubations were performed in the absence of serum. In contrast, incubation of GBS type III antigen with serum deficient in antibody to GBS resulted in a marked enhancement of PMN attachment to human endothelial cells. No significant enhancement of adherence was seen with the antigen in the presence of serum containing GBS type III antibody. These data suggest that the GBS type III antigen by itself may inhibit the influx of PMNs into the local site of infection in the alveoli. In contrast, when exposed to blood components within the vascular space, the antigen may promote PMN adhesion to the endothelium, potentially contributing to pulmonary hypertension, edema, and respiratory failure in this most fulminant of bacterial pulmonary infections of the neonate.