Effects of alpha- and beta-adrenergic agonists on Toxoplasma gondii infection in murine macrophages
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Updated: Aug 18, 2026

Toxoplasma gondii Cyst Wall Formation in Activated Bone Marrow-derived Macrophages and Bradyzoite Conditions
Published on: August 12, 2010
Julie Gets1, Fernando P Monroy
1Department of Biological Sciences, Northern Arizona University, PO Box 5640, Flagstaff, Arizona 86011, USA.
Abstract:
We investigated the effects of alpha- and beta-adrenergic receptor agonists on the ability of Toxoplasma gondii to infect and proliferate in cultured murine macrophages. Macrophages pretreated in vitro with varying concentrations of alpha- and beta-adrenergic agonists and incubated with the RH strain of T. gondii did not result in a significant increase in the percentage of infected macrophages compared with negative controls. When parasites were pretreated with L-phenylephrine, an alpha-agonist, and L-isoproterenol, a beta-agonist, before infection, there was no significant change in the percentage of infected macrophages. Clonidine, an alpha2-adrenergic agonist, led to a significant decrease in the number of infected macrophages at all concentrations tested. The effects of clonidine were blocked by yohimbine, a specific alpha2-adrenergic antagonist, but not by phentolamine, an alpha1-adrenergic antagonist. These results suggest that the antiparasitic effects exhibited by clonidine (alpha2-adrenergic agonist) are mediated through an alpha2-adrenoreceptor found on the surface of T. gondii.

