PULMONARY SURFACTANT PROTEINS A AND D AND MYCOBACTERIA

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 结核病是一种传染病，影响着世界30%的人口。最近的研究表明，当微生物被吸入时，肺内的两种蛋白质可以迅速与其相互作用。这些蛋白质被命名为SP-A和SP-D。SP-A蛋白似乎与细菌结合在一起，使其能够避免免疫系统的识别和破坏。相比之下，SP-D蛋白似乎也结合了引起结核病的细菌，并促进了它的破坏。目前，我们对SP-A和SP-D控制这些细菌与杀死细菌所需的肺细胞相互作用的细节知之甚少。这项研究的目的是使用SP-A和SP-D的制剂详细检查这些相互作用，SP-A和SP-D是引起结核病的细菌和从人肺中分离出来的细胞，它们是杀死微生物所必需的。为了在这些研究中使用正确类型的人肺细胞，我们用生理盐水冲洗人肺的一小部分，并回收细胞。该项目的长期目标是寻找方法，增强SP-D导致细菌杀灭的能力，并削弱SP-A的能力，减少对细菌的杀灭。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Tuberculosis is an infectious disease that affects 30% of the world population. Recent work suggests that two proteins within the lung can rapidly interact with the microorganism when it is inhaled. These proteins are named SP-A and SP-D. The SP-A protein appears to bind the bacteria and enable it to avoid recognition and destruction by the immune system. In contrast, the SP-D protein also appears to bind the tuberculosis causing bacteria and facilitate its destruction. We currently understand few of the details by which the SP-A and SP-D control the interactions of these bacteria with lung cells that are required for killing the bacteria. The purpose of this study is to examine these interactions in detail using preparations of SP-A and SP-D, tuberculosis causing bacteria and cells isolated from human lungs, that are required for the killing of the organism. In order to use the correct type of human lung cells for these studies we rinse small segments of human lung with a saline solution and recover the cells. The long-term goals of this project are to find ways to enhance the ability of SP-D to cause the killing of the bacteria and diminish the ability of SP-A reduce the killing of the bacteria.