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Date of Award

Spring 2005

Document Type

Restricted Thesis: Campus only access

Degree Name

Bachelor of Science



First Advisor

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.