title: Infection with Toxoplasma gondii increases atherosclerotic lesion in ApoE-deficient mice.
abstract: 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.
authors.affiliation: Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
authors.forename: Luciane R
authors.initials: LR
authors.lastname: Portugal
authors.forename: Luciana R
authors.initials: LR
authors.lastname: Fernandes
authors.forename: Giovana C
authors.initials: GC
authors.lastname: Cesar
authors.forename: Helton C
authors.initials: HC
authors.lastname: Santiago
authors.forename: Dirce R
authors.initials: DR
authors.lastname: Oliveira
authors.forename: Neide M
authors.initials: NM
authors.lastname: Silva
authors.forename: Andrea A
authors.initials: AA
authors.lastname: Silva
authors.forename: Joseli
authors.initials: J
authors.lastname: Lannes-Vieira
authors.forename: Rosa M E
authors.initials: RM
authors.lastname: Arantes
authors.forename: Ricardo T
authors.initials: RT
authors.lastname: Gazzinelli
authors.forename: Jacqueline I
authors.initials: JI
authors.lastname: Alvarez-Leite
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism / Q000469:parasitology / Q000473:pathology; D001057:Apolipoproteins E / Q000235:genetics* / Q000378:metabolism; D001161:Arteriosclerosis / Q000209:etiology*; D018932:Chemokine CCL2 / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D007371:Interferon-gamma / Q000378:metabolism; D008074:Lipoproteins / Q000097:blood; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D009573:Nitrites / Q000097:blood; D018384:Oxidative Stress; D014122:Toxoplasma / Q000276:immunology / Q000472:pathogenicity*; D014124:Toxoplasmosis, Animal / Q000150:complications*
chemical_list: D001057:Apolipoproteins E; D018932:Chemokine CCL2; D008074:Lipoproteins; D009573:Nitrites; D007371:Interferon-gamma; D002784:Cholesterol; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse