MECHANISMS OF HOST RESISTANCE TO GROUP B STREPTOCOCCI

B组链球菌仍然是发病和死亡的重要原因 人类新生儿和其他免疫受损宿主的死亡率。虽然 在了解寄主的机制方面取得了长足的进步。 对这些生物的防御，我们还不太了解 关于这种最猛烈的细菌感染的发病机制。我们 希望着重从三个方面阐述其发病机制和免疫机制 B组链球菌感染，我们认为有令人兴奋的潜力。 首先，我们将试图确定纤维连接蛋白(FN)在 促进上皮细胞对B群链球菌的黏附。此外, 我们将确定FN如何增强多克隆和 单抗。第二，我们将确定严重的中性粒细胞减少症 和骨髓粒细胞储备库耗尽在人类和 实验动物B组疾病是减产的结果 来自补体的白细胞动员因子，如C3E 系统。最后，我们将确定B组链球菌或其可溶性 产品影响血管内皮细胞-中性粒细胞的相互作用， 从而促成了本病肺损伤的严重和发病机制。 常常压倒细菌感染。

Group B streptococci continue to be a significant cause of morbidity and mortality in human neonates and other immunocompromised hosts. Although great strides have been made in understanding the mechanisms of host defense against these organisms, we still do not understand a great deal about the pathogenesis of this most fulminant of bacterial infections. We wish to concentrate on three aspects of the pathogenesis of, and immunity to group B streptococcal infection that we feel have exciting potential. First, we will seek to determine exactly what role fibronectin (FN) has in promoting epithelial cell adherence to group B streptococci. In addition, we will determine how FN enhances the opsonic activity of polyclonal and monoclonal antibody. Second, we will determine if the profound neutropenia and marrow granulocyte store depletion commonly observed in human and experimental animal group B disease is the result of decreased production of leukocyte mobilizing factors, such as C3e, derived from the complement system. Lastly, we will determine if group B streptococci or their soluble products affect vascular endothelial cell-neutrophil interactions and, thus, contribute to the pathogenesis of the lung damage in this serious and often overwhelming bacterial infection.