MECHANISMS OF HOST RESISTANCE TO GROUP B STREPTOCOCCI

B族链球菌仍然是发病的重要原因， 人类新生儿和其他免疫功能低下宿主的死亡率。 虽然 在理解宿主的机制方面已经取得了很大的进展， 防御这些生物体，我们仍然不了解很多 关于这种最具爆发性的细菌感染的发病机制。 我们 我想集中讨论三个方面的发病机制，和免疫 B族链球菌感染，我们觉得有令人兴奋的潜力。 首先，我们将试图确定纤维连接蛋白（FN）在 促进上皮细胞与B族链球菌的粘附。 此外，本发明还提供了一种方法， 我们将确定FN如何增强多克隆和 单克隆抗体 其次，我们将确定是否严重的中性粒细胞减少症 和骨髓粒细胞库耗竭， 实验动物B组疾病是由于产量下降 白细胞动员因子，如C3 e，来源于补体 系统 最后，我们将确定B组链球菌或其可溶性 产物影响血管内皮细胞-嗜中性粒细胞的相互作用， 因此，有助于肺损伤的发病机制，在这种严重的， 通常是压倒性的细菌感染。

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.