Honors Theses
Date of Award
2012
Document Type
Undergraduate Thesis
Department
Chemistry and Biochemistry
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 IFN- y, and are more sensitive to the cytokine-stimulating hormone angiotensin II (ANGII). To test this hypothesis, T lymphocytes were isolated from control and SLE mice, and cytokine 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: A Potential Link Between Inflammation and Hypertension in SLE" (2012). Honors Theses. 1941.
https://egrove.olemiss.edu/hon_thesis/1941
Accessibility Status
Searchable text