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Infection and Immunity, June 2004, p. 3571-3576, Vol. 72, No. 6
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.6.3571-3576.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Infection with Toxoplasma gondii Increases Atherosclerotic Lesion in ApoE-Deficient Mice

Luciane R. Portugal,1 Luciana R. Fernandes,1 Giovana C. Cesar,1 Helton C. Santiago,1 Dirce R. Oliveira,1 Neide M. Silva,2 Andrea A. Silva,3 Joseli Lannes-Vieira,3 Rosa M. E. Arantes,4 Ricardo T. Gazzinelli,1,5 and Jacqueline I. Alvarez-Leite1*

Department of Biochemistry and Immunology,1 Department of Pathology, Institute of Biological Sciences, Federal University of Minas Gerais,4 Laboratory of Immunopathology, René Rachou Research Center, Oswaldo Cruz Foundation, Belo Horizonte,5 Immunoparasitology Laboratory, Biomedical Sciences Institute, Federal University of UberlÂndia, UberlÂndia, Minas Gerais,2 Department of Immunology, Institute Oswaldo Cruz, Oswaldo Cruz Foundation, Rio de Janeiro, Rio de Janeiro, Brazil3

Received 25 September 2003/ Returned for modification 1 December 2003/ Accepted 19 February 2004

Toxoplasma gondii is an intracellular protozoan that elicits a potent inflammatory response during the acute phase of infection. Herein, we evaluate whether T. gondii infection alters the natural course of aortic lesions. ApoE knockout mice were infected with T. gondii, and at 5 weeks of infection, serum, feces, and liver cholesterol; aortic lesion size, cellularity, and inflammatory cytokines; and levels of serum nitrite and gamma interferon (IFN-{gamma}) were analyzed. Our results showed that serum cholesterol and atherogenic lipoproteins were reduced after T. gondii infection. The reduction of serum levels of total cholesterol and atherogenic lipoproteins was associated with increases in the aortic lesion area, numbers of inflammatory cells, and expression of monocyte chemoattractant protein 1 and inducible nitric oxide synthase mRNA in the site of lesions as well as elevated concentrations of IFN-{gamma} and nitrite in sera of T. gondii-infected animals. These results suggest that infection with T. gondii accelerates atherosclerotic development by stimulating the proinflammatory response and oxidative stress, thereby increasing the area of aortic lesion.

* Corresponding author. Mailing address: Laboratório de Bioquímica Nutricional, Departamento of Bioquimica e Imunologia, ICB—UFMG, Caixa Postal 486, 30161-970, Belo Horizonte, MG, Brazil. Phone: 55-31-34992652. Fax: 55-31-34415963. E-mail: alvarez{at}ufmg.br.

Editor: J. F. Urban, Jr.

Infection and Immunity, June 2004, p. 3571-3576, Vol. 72, No. 6
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.6.3571-3576.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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