J R Campbell1, M S Edwards. 1. Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA.
Abstract
UNLABELLED: 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-alpha (TNF-alpha), 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-alpha, 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-alpha- 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.
UNLABELLED: 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-alpha (TNF-alpha), 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-alpha, 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-alpha- 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.
Authors: Ofer Levy; Rochelle M Jean-Jacques; Colette Cywes; Richard B Sisson; Kol A Zarember; Paul J Godowski; Jennifer L Christianson; Hilde-Kari Guttormsen; Michael C Carroll; Anne Nicholson-Weller; Michael R Wessels Journal: Infect Immun Date: 2003-11 Impact factor: 3.441