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Pulmonary Arterial Hypertension (PAH) is a disease associated with high blood pressure specifically in the lung circulation. Symptoms include dyspnea and cyanosis, and the mean survival post-diagnosis is 2.8 years without treatment. PAH can be characterized by accumulating vascular damage which results in lesion formation causing a decrease in the diameter of vessels, obstruction of flow, and ultimately increased pressure on the right heart leading to failure. These lesions define an arteriopathy that is a hallmark of PAH which is, in part, dependent on infiltration of inflammatory cells into the vascular wall. PAH presents uniquely in males and females with females being diagnosed more often than males, but with males having a much worse prognosis than females. We recently reported that in the SUGEN/Hypoxia model of PAH there is increased circulating MCP-1 and GM-CSF, indicative of macrophage-driven infiltration. Further we found that CXCL-10 was increased in females, indicative of T-cell infiltration. We hypothesized that males would exhibit macrophage expression in the vascular wall, whereas females would have T-cell infiltration. Following histological staining of both male and female samples our preliminary data suggests females exhibit more T cells and male exhibit more macrophages. This data suggests unique inflammatory cell phenotypes that correlate with sex in PH.

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Medicine and Health Sciences

The Role of Inflammatory Cells in the Sex Dimorphism of Pulmonary Arterial Hypertension