Effects of α- and β-adrenergic agonists on Toxoplasma gondii infection in murine macrophages

We investigated the effects of alpha- and beta-adrenergic receptor agonists on the ability of Toxoplasma gondii to infect and proliferate in Cultured murine rnacrophages. 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 inacrophages 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 inacrophages. Clonidine, all alpha(2)-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 alpha(2)-adrenergic antagonist, but not by phentolamine, an alpha(1)-adrenergic antagonist. These results suggest that the antiparasitic effects exhibited by clonidine (a2-adrenergic agonist) are mediated through an alpha(2)-adrenoreceptor found oil the surface of T gondii.