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Date of Award

Spring 2013

Document Type

Restricted Thesis: Campus only access

Degree Name

Bachelor of Science


Biochemistry & Molecular Biol.

First Advisor

Dr. Krista Stenger


Macrophages play an integral role in eliminating infection during the inflammatory response. Catecholamines are known to alter macrophage function by binding to adrenergic receptors on the macrophage membrane. Stimulation through β-adrenergic receptors (β-AR) is known to decrease macrophage function while stimulation through the α-adrenergic receptor (α-AR) is thought to have a stimulatory effect on immune function. The RAW264.7 murine macrophage cell line is used as a model of macrophage function, but little is known about the expression of adrenergic receptors on these cells. In these studies, macrophages were treated with the catecholamine norepinephrine, the non-selective α-adrenergic receptor agonist clonidine, or the selective α2-adrenergic receptor antagonist RS79948 (RS), prior to lipopolysaccharide (LPS) activation, and then analyzed for the production of the proinflammatory cytokines TNF-α and IL-6. Low concentrations of clonidine increased cytokine production while RS reversed these effects. Immunocytochemistry and western blot analysis were used to examine adrenergic receptor expression on the macrophages. These studies demonstrate that RAW264.7 macrophages express α2-adrenergic receptors on their surface. Activation with LPS and exposure to low concentrations of agonist may also enhance receptor expression. These findings suggest that differences in adrenergic receptor expression on macrophages are important determinants that influence the response of macrophages to catecholamines, and provide evidence to support a stimulatory effect on cytokine production when catecholamines bind to the α2-adrenergic receptors.