MECHANISMS OF HOST RESISTANCE TO GROUP B STREPTOCOCCI

描述（改编自申请人摘要）：当前提案将 探讨细胞因子在B族链球菌（GBS）应答中的作用 在体外和体内的实验模型。 研究旨在 检查肿瘤坏死因子α的连续出现。 （TNFa）， IL-1 β（IL-1b）、IL-6和IL-8在体外暴露于人 单核细胞感染GBS 这些细胞因子的相继出现将 也可在新生大鼠接种GBS后进行评估。 我们将 通过关键的RGD序列检查纤连蛋白（FN）的作用， 诱导或增强人单核细胞的TNF α释放 B群链球菌。 C5 a作为辅助因子沿着GBS在 还将探索在体外引起细胞因子释放。 这些研究将 包括旨在确定GBS C5 a-ase是否可以影响C5 a的实验 诱导或增强TNF α释放。 这些研究应该会产生数据 这将有助于解释促炎细胞因子在 感染性休克的发病机制，由于这种最暴发性形式的新生儿 细菌感染

DESCRIPTION (Adapted from applicant's abstract): The current proposal will explore the role of cytokines in the response to group B streptococci (GBS) in vitro and in vivo in an experimental model. Studies are designed to examine the sequential appearance of tumor necrosis factor alpha. (TNFa), IL-1 beta (IL-1b), IL-6, and IL-8 following in vitro exposure of human mononuclear cells to GBS. The sequential appearance of these cytokines will also be assessed following GBS inoculation of neonatal rats. We will examine the role of fibronectin (FN) through the critical RGD sequence, in inducing or enhancing TNFa release by human mononuclear cells exposed to group B streptococci. The role of C5a as a co-factor along with GBS in causing cytokine release in vitro will also be explored. These studies will include experiments designed to determine if the GBS C5a-ase can affect C5a induction or enhancement of TNFa release. These studies should yield data that will help to explain the role of the proinflammatory cytokines in the pathogenesis of septic shock due to this most fulminant form of neonatal bacterial infection.