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. This project focuses on the mechanism of intestinal and lung cell damage in response to decreased blood flow (ischemia). Ischemia induces immediate organ damage that is magnified with the return of blood flow (reperfusion). The exposed cells in the intestine are critical for maintaining an intact barrier in the host defense against pathogens;thus, molecules involved in ischemia/reperfusion-induced intestinal injury may also provide targets for pathogen recognition. Intestinal cell damage due to ischemia and subsequent reperfusion events is mediated by immune cells and systems. However, the exact mechanisms of either process are unknown, and other innate immune molecules are likely to be involved. Molecules called toll-like receptors are candidates for involvement. The long term goal of this project is to understand the extent that expression of toll-like receptors on the intestinal cells contributes to damage of these cells. The central hypothesis of this project is that specific toll-like receptors cause intestinal inflammation associated with cellular damage induced by ischemia/reperfusion and other related injuries. These studies will provide critical data to improve our understanding of ischemia/reperfusion injury that occurs not only in the intestine, but also during heart attacks and strokes.
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