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细胞因子增强B族链球菌III型的调理吞噬作用。

Cytokines enhance opsonophagocytosis of type III group B Streptococcus.

作者信息

Campbell J R, Edwards M S

机构信息

Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA.

出版信息

J Perinatol. 2000 Jun;20(4):225-30. doi: 10.1038/sj.jp.7200360.

DOI:10.1038/sj.jp.7200360
PMID:10879334
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.

摘要

未标记

中性粒细胞(多形核白细胞(PMN)介导的杀伤作用对宿主抵御B族链球菌III型(GBS)至关重要。在新生儿中,PMN介导的宿主防御在质量和数量上的缺陷可能导致新生儿对这种病原体的反应受损。

目的

本研究的目的是确定肿瘤坏死因子-α(TNF-α)、粒细胞集落刺激因子(G-CSF)或粒细胞-巨噬细胞集落刺激因子(GM-CSF)是否会增强新生儿PMN介导的对GBS III型的杀伤作用。

研究设计

将来自成人或新生儿的PMN与TNF-α、G-CSF或GM-CSF一起孵育;接下来,在体外调理吞噬试验中评估PMN介导的对GBS III型的杀伤作用。

结果

在向反应混合物中添加GBS之前,用这些细胞因子处理PMN 5分钟,可增强成人PMN和新生儿PMN对细菌的调理吞噬作用。对于TNF-α和GM-CSF处理的成人PMN以及GM-CSF处理的新生儿PMN,这种作用具有统计学意义。GM-CSF处理的PMN对GBS III型的增强杀伤作用通过FcRIII的单克隆抗体阻断而降低。

结论

G-CSF在体外增强新生儿PMN介导的对GBS III型的杀伤作用。这些研究表明,FcRIII受体的使用可能是GM-CSF增强PMN介导的对GBS III型杀伤作用的一种机制。添加含有GBS III型特异性抗体的纯化免疫球蛋白G可促进GM-CSF处理的PMN的调理吞噬作用。我们推测,单独给予GM-CSF或与静脉注射免疫球蛋白联合使用可能会改善新生儿宿主对GBS III型的反应。

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