2024-04-172024-04-172024-03-21https://hdl.handle.net/20.500.12503/32694In the United States, strokes are one of the leading causes of death- with ischemic strokes being the most common. The etiology by which ischemic strokes occur may be due to large vessel occlusion. Typically, this process occurs by which a thrombus or embolus occludes a major vessel within the brain leading to reduced blood flow (ischemia) precipitating damage to brain tissue. Large vessel occlusion is a critical event, in which a rapid response is required to ensure the survival of brain tissue. It is understood that IFN-gamma is involved in the production of various inflammatory mediators, however, in the context of the stroke, it is not known where the IFN-gamma production is sourced from early in the stroke cascade. This study investigates the production of IFN-gamma in the context of a large vessel occlusion in mice. In vitro and in vivo studies were utilized to (1) compare the production of IFN-gamma amongst large vessel pre-occlusion, large vessel post-occlusion, and a distal vascular site (2) examine the direct relationship between oxygen-glucose deprivation applied to mixed cortical cultures and naïve lymphocytes (3) investigate the source of IFN-gamma production. Collected data was analyzed by utilizing flow cytometry. Findings revealed that in comparison to the pre-occlusion, the post-occlusion sample of blood contained increased levels of IFN-gamma. Mixed cortical cultures were examined under ischemic-like conditions and demonstrated increased IFN-gamma production from naïve cells. Evidence also suggested that the most likely source of IFN-gamma production stems from macrophages. IFN-gamma could potentially be an important modulator in the exacerbation of brain parenchymal damage, especially in the context of post-large vessel occlusion.enposter