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Cytokines enhance opsonophagocytosis of type III group B Streptococcus
1Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA.
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.
Insights
Granulocyte-macrophage colony-stimulating factor (GM-CSF) enhances neonatal neutrophil killing of Group B Streptococcus (GBS). This suggests GM-CSF, potentially with immunoglobulin therapy, could improve infant defense against GBS infections.
Area of Science:
- Immunology
- Neonatal Medicine
- Infectious Disease
Background:
- Neutrophil (polymorphonuclear leukocyte, PMN) mediated killing is crucial for host defense against Group B Streptococcus (GBS).
- Neonates often exhibit impaired PMN function, contributing to susceptibility to GBS infection.
Purpose of the Study:
- To investigate if cytokines like TNF-alpha, G-CSF, or GM-CSF can enhance neonatal PMN-mediated killing of type III GBS.
- To assess the role of FcRIII receptors in GM-CSF-augmented PMN killing of GBS.
Main Methods:
- Adult and neonatal PMNs were incubated with TNF-alpha, G-CSF, or GM-CSF.
- PMN-mediated killing of type III GBS was evaluated using an in vitro opsonophagocytic assay.
- FcRIII receptor involvement was tested using monoclonal antibody blockade.
Main Results:
- Cytokine treatment (TNF-alpha, G-CSF, GM-CSF) enhanced GBS killing by both adult and neonatal PMNs.
- GM-CSF significantly improved killing by neonatal PMNs.
- GM-CSF's effect was partially mediated by FcRIII receptors and enhanced by specific antibodies.
Conclusions:
- Granulocyte-colony stimulating factor (G-CSF) enhances neonatal PMN-mediated killing of GBS in vitro.
- GM-CSF augments PMN killing of GBS, potentially via FcRIII receptors.
- GM-CSF, possibly combined with intravenous immunoglobulin, may improve neonatal host defense against GBS.