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

Julie Getz, Fernando P Monroy

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

We investigated the effects of α- and β-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 α- and β-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 α-agonist, and L-isoproterenol, a β-agonist, before infection, there was no significant change in the percentage of infected macrophages. Clonidine, an α2-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 α2-adrenergic antagonist, but not by phentolamine, an α1-adrenergic antagonist. These results suggest that the antiparasitic effects exhibited by clonidine (α2-adrenergic agonist) are mediated through an α2-adrenoreceptor found on the surface of T. gondii.

Original languageEnglish (US)
Pages (from-to)193-195
Number of pages3
JournalJournal of Parasitology
Volume91
Issue number1
DOIs
StatePublished - Feb 2005

Fingerprint

adrenergic agonists
Adrenergic Agonists
Toxoplasmosis
Toxoplasma gondii
clonidine
macrophages
Macrophages
Toxoplasma
Clonidine
adrenergic antagonists
mice
agonists
Adrenergic Antagonists
infection
parasite
yohimbine
Antiparasitic Agents
phenylephrine
Yohimbine
Phentolamine

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Parasitology
  • Microbiology

Cite this

Effects of α- and β-adrenergic agonists on Toxoplasma gondii infection in murine macrophages. / Getz, Julie; Monroy, Fernando P.

In: Journal of Parasitology, Vol. 91, No. 1, 02.2005, p. 193-195.

Research output: Contribution to journalArticle

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