Honors Theses
Date of Award
2012
Document Type
Undergraduate Thesis
Department
Biology
First Advisor
Mika Jekabsons
Relational Format
Dissertation/Thesis
Abstract
The disease Systemic Lupus Erythematosus is a chronic inflammatory, autoimmune disorder that primarily affects women during their reproductive years. Women with SLE are at a greater risk of developing hypertension, which increases their risk of mortality from a cardiac related event. A proposed mechanism for SLE hypertension suggests that inflammation in the kidneys causes renal dysfunction, presumably resulting in less water excretion, increased plasma volume, and thus high blood pressure. This experiment tests the hypothesis that the T-cells from a mouse model of SLE hyper secrete the inflammatory cytokines IL-17, IL-10, and DFN- y, and are more sensitive to the cytokine-stimulating hormone angiotensin II (ANG II). To test this hypothesis, T lymphoc}^es were isolated from control and SLE mice, and cj^okine secretion into the culture media was determined in the presence or absence of ANG II. Thymocytes from SLE mice secreted greater levels of all three inflammatory cytokines, although excess IL-17 secretion occurred only after the onset of renal damage. Angiotensin II increased production of IFN- y, but there was no major difference between the SLE and Control groups. These results indicate that hyper secretion of IL-17, IL-10, and IFN- y by SLE T-cells may be contributing to renal inflammation, kidney damage, and therefore SLE hypertension. T-cell hypersensitivity to ANG II could not account for the hypertension, suggesting that these cells are excessively sensitive to another factor (that is present in the culture media) or have an innately higher secretion rate.
Recommended Citation
Aujla, Khush Singh, "Angiotensin II as a Potential Regulator of Inflammatory Cytokines in Inducing Hypertension in Systemic Lupus Erythematosus" (2012). Honors Theses. 2172.
https://egrove.olemiss.edu/hon_thesis/2172
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