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Experimental Parasitology 123 (2009) 65–72

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Experimental Parasitology
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Toxoplasma gondii: The role of IFN-gamma, TNFRp55 and iNOS in inflammatory changes during infection
Neide Maria Silva a,*, Júlio César Menezes Vieira b, Claudia Martins Carneiro d, Wagner Luiz Tafuri c

ImmunopathologyLaboratory, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, 38 400-902, Uberlândia, Minas Gerais, Brazil Department of Biochemistry and Immunology, Federal University of Minas Gerais, 31270-010, Belo Horizonte, MG, Brazil c Department of Pathology, Federal University of Minas Gerais, 31270-010, Belo Horizonte, MG, Brazil d Department of Clinical Analysis, Universidade Federal deOuro Preto, 35400-000, Ouro Preto, Minas Gerais, Brazil

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In order to examine the role of IFN-c, TNFRp55 and iNOS in inflammatory reaction during toxoplasmosis, IFN-cÀ/À, TNFRp55À/À and iNOSÀ/À mice were experimentally infected with Toxoplasma gondii ME-49 strain. The organs of the mice were evaluated for histology and immunohistochemistry in detectionof tissue parasitism and iNOS positive cells. IFN-cÀ/À mice presented mild inflammation in peripheral organs associated with a high parasitism and mortality in the acute phase of infection. In contrast, the peripheral organs of WT, TNFRp55À/À and iNOSÀ/À mice, presented a significant inflammatory reaction and low tissue parasitism in the same period of infection. The inflammatory lesions and tissueparasitism were increased and more severe in the Central Nervous System (CNS) of TNFRp55À/À and iNOSÀ/À with a progression of infection, when compared to WT mice. In these knockout animals, the inflammatory changes were associated with low levels or no expression of iNOS in TNFRp55À/À and iNOSÀ/À mice, respectively. Ó 2009 Elsevier Inc. All rights reserved.

Article history: Received 6 December2008 Received in revised form 4 April 2009 Accepted 26 May 2009 Available online 6 June 2009 Keywords: IFN-c Inflammation iNOS Protozoa Toxoplasma gondii TNFRp55

1. Introduction Toxoplasma gondii infection in most adult animals and humans is asymptomatic because of effective protective immunity (Frenkel, 1988). In immunocompetent individuals, infection with the parasite causes little or no overtsigns of disease in its hosts, but in situations of immunodeficiency, or during congenital infection, T. gondii may emerge as a serious infection, which if untreated can lead to host death (Denkers and Gazzinelli, 1998; Denkers, 1999). Tachyzoites are the principal pathogenic stage in toxoplasmosis. If immunity is not acquired in a timely fashion, tachyzoites continue to multiply, destroying anexcessive number of cells and producing lesions in several organs, with pneumonia and encephalitis being the prominent causes of illness and death (Frenkel, 1988). In immunocompromised individuals, in particular those with AIDS, the rapid multiplication of tachyzoites in the central nervous system (CNS) on reactivation of infection results in toxoplasmic encephalitis (TE) (Kasper and Buzoni-Gatel,1998). Virtually all mouse strains develop a strong Th1 immune response to T. gondii, regardless of whether they present resistant or susceptible MHC haplotypes (Gazzinelli et al., 1991, 1992). In murine models, CD4+ and CD8+ T cells have both important roles in resistance to T. gondii, which is at least in part mediated by cyto* Corresponding author. Fax: +55 34 3218 2333. E-mail (N.M. Silva). 0014-4894/$ - see front matter Ó 2009 Elsevier Inc. All rights reserved. doi:10.1016/j.exppara.2009.05.011

kines (Suzuki and Remington, 1988; Gazzinelli et al., 1991). In vivo studies indicate that IFN-c is a major cytokine, which mediates resistance against T. gondii infection (Suzuki et al., 1988). In vitro experiments have shown a crucial role for both IFN-c and...
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