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Date of Award
Restricted Thesis: Campus only access
Bachelor of Science
Dr. Krista Stenger
It has been established that macrophages release inflammatory mediators known as cytokines upon LPS-stimulation. Previous studies suggest that catecholamines alter cytokine production, such as tumor necrosis factor-a (TNF-a) or interleukin-l β (IL-l β) by binding to a- or β- adrenergic receptors on macrophage cell membranes. This study was designed to determine whether interleukin-6 (IL-6) production was affected by catecholamines. Also, studies were performed to identify which adrenergic receptor (or both) was responsible for altering IL-6 production. Treatment with a low concentration of norepiniphrine (NE) (1 OnM) increased the LPS-stimulated production of IL-6. Treatment with NE in the presence of the alpha adrenergic antagonist, yohimbine, resulted in a decrease in LPS-stimulated IL-6 release compared to levels produced in the absence of the antagonist. Treatment with NE in the presence of the P-adrenergic receptor antagonist, ICI118,551, had no effect on the NE induced increase in LPS-stimulated production ofiL-6 when compared to levels produced in the absence of the antagonist. These findings suggest that LPS-induced production ofinterleukin-6 by macrophages may be regulated by NE. Further investigation is needed to understand the role catecholamines play on cytokine production and how these molecules may regulate the immune response.
Callison, Andrew R., "The effect of norepinephrine on the production of interleukin-6 (IL-6) in the raw 264.7 macrophage cell line" (2005). Honors Theses. 365.