Cytokines Enhance Opsonophagocytosis of Type III Group B Streptococcus

Abstract

Neutrophil (polymorphonuclear leukocyte (PMN))-mediated killing is important to host defense against type III group B Streptococcus (GBS). In neonates, a qualitative and quantitative deficiency in PMN-mediated host defense may contribute to an impaired neonatal response to this pathogen.

OBJECTIVE:

The purpose of this study was to determine whether tumor necrosis factor-α (TNF-α), granulocyte colony-stimulating factor (G-CSF), or granulocyte-macrophage colony-stimulating factor (GM-CSF) would enhance neonatal PMN-mediated killing of III GBS.

STUDY DESIGN:

PMNs from adults or neonates were incubated with TNF-α, G-CSF, or GM-CSF; next, PMN-mediated killing of III GBS was assessed in an in vitro opsonophagocytic assay.

RESULTS:

Treatment of PMNs with these cytokines for an interval of 5 minutes before addition of GBS to the reaction mixture enhanced opsonophagocytosis of bacteria both by adult PMNs and neonatal PMNs. The effect was statistically significant for TNF-α- and GM-CSF-treated adult PMNs and for GM-CSF-treated neonatal PMNs. The enhanced killing of III GBS by GM-CSF-treated PMNs was reduced by monoclonal antibody blockade of FcRIII.

CONCLUSION: G-CSF enhances the neonatal PMN-mediated killing of III GBS in vitro. These studies suggest that use of FcRIII receptors may be one mechanism by which GM-CSF augments the PMN-mediated killing of III GBS. The addition of purified immunoglobulin G containing III GBS-specific antibody facilitated opsonophagocytosis by GM-CSF-treated PMNs. We

speculate that the administration of GM-CSF alone or in combination with intravenous immunoglobulin may improve the neonatal host response to III GBS.