INFLAMMATION IN RESISTANCE TO BACTERIAL INFECTION

兼性细胞内病原体，如 结核病、麻风病和利什曼病仍然是一个严重的威胁 对人类健康的影响。 一个有价值的和广泛使用的实验室模型， 宿主-病原体相互作用的实验感染提供了 小鼠与兼性细胞内细菌单核细胞增生李斯特菌。 一般认为免疫激活的巨噬细胞 是唯一能杀死L.单核细胞增多症 相比 然而，这一假设，这位研究人员最近的报告， 表明其他细胞类型（即炎性中性粒细胞和 巨噬细胞）也能杀死L.单核细胞增生症，而且这是 宿主有效地将炎性吞噬细胞动员到 对疾病的结果至关重要的淋病感染。 这 随后的实验证实了这一假设， 李斯特菌免疫T细胞可以将增强的抵抗力转移到 嗜中性粒细胞增多和炎性中性粒细胞积聚能力增加 和巨噬细胞。 本研究的目的是分析 炎性反应有助于抵抗炭疽病。 到 实现这一目标的影响，细胞数量，路线，和时间的 李斯特菌免疫T细胞的过继转移 增强的抗真菌能力和增加的炎性 将测定T细胞的Lyt反应性以及Lyt表型 负责调节这些现象。 不同的近交系小鼠品系 在他们的C5水平将被用作一种工具，以确定的作用， 补体在T细胞介导的抗血小板减少症和增强 炎症反应。 炎症作用的直接证据 将通过体内实验提供抗真菌性， 将决定炎症对L. 单核细胞增多症在体外存活。

Facultative intracellular pathogens, such as the causative agents of tuberculosis, leprosy, and leischmaniasis, continue to be a serious threat to human health. A valuable and widely used laboratory model for this type of host-pathogen interaction has been provided by experimental infection of mice with the facultative intracellular bacterium Listeria monocytogenes. It generally has been assumed that immunologically-activated macrophages are the only cells capable of killing L. monocytogenes. In contrast to this assumption, however, recent reports by this investigator have suggested that other cell types (i.e. inflammatory neutrophils and macrophages) also can kill L. monocytogenes, and that it is the ability of the host to efficiently mobilize inflammatory phagocytes to sites of listeria infection that is critical to the outcome of the disease. This hypothesis has been strengthened by subsequent experiments which have shown that Listeria-immune T cells can transfer both enhanced resistance to listeriosis and an increased ability to accumulate inflammatory neutrophils and macrophages. The purpose of this research will be to analyze how the inflammatory response contributes to resistance to listeriosis. To accomplish this goal the effects of cell number, route, and timing of administration of Listeria-immune T cells on the adoptive transfer of both enhanced resistance to listeriosis and increased inflammatory responsiveness will be determined, as will the Lyt phenotype of the T cells responsible for mediating these phenomena. Inbred mouse strains which vary in their levels of C5 will be used as a tool to identify the role of complement in both T cell-mediated resistance to listeriosis and enhanced inflammatory responsiveness. Direct evidence for the role of inflammation in resistance to listeriosis will be provided by in vivo experiments which will determine the effects of inflammation on the ability of L. monocytogenes to survive in vitro.