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Taenia crassiceps antigens induce a Th2 immune response and attenuate injuries experimentally induced by neurotoxoplasmosis in BALB/c mice
Authors:Amanda J.S. Souza  Anália C. Milhomem  Hanstter H.A. Rezende  Hidelberto Matos-Silva  Marina C. Vinaud  Milton A.P. Oliveira  Ana M. Castro  Ruy S. Lino-Júnior
Affiliation:1. Department of Microbiology, Immunology, Parasitology and Pathology, Tropical Pathology and Public Health Institute, Federal University of Goias, Rua 235 S/N, Setor Universitário, 74605-050 Goiânia, Goiás, Brazil;2. Medicine Faculty, UNIRG – Univeristy Center, Avenida Antônio Nunes da Silva n° 2195, Pq. das Acácias, 77425-500 Gurupi, Tocantins, Brazil
Abstract:Toxoplasma gondii is a pathogenic agent responsible for causing both systemic and local disease which elicits a typically pro-inflammatory, Th1 immune response. Taenia crassiceps antigen induces a Th2 immune response that immunomodulates Th1 based infections. Therefore the aim of this study was to evaluate whether T. crassiceps cysticerci antigens are able to modulate the inflammatory response triggered in experimental neurotoxoplasmosis (NT). BALB/c mice were inoculated with T. gondii cysts and/or cysticerci antigens and euthanized at 60 and 90 days after inoculation (DAI). The histopathology of the brains and cytokines produced by spleen cells culture were performed. The animals from the NT group, 90DAI (NT90), presented greater intensity of lesions such as vasculitis, meningitis and microgliosis and cytokines from Th1 profile characterized by high levels of IFN-gamma. While in the T. crassiceps antigens group, 60DAI, there were more discrete lesions and high levels of IL-4, a Th2 cytokine. In the NT co-inoculated with cysticerci antigens group the parenchyma lesions were more discrete with lower levels of IFN-gamma and higher levels of IL-4 when compared to NT90. Therefore the inoculation of T. crassiceps antigens attenuated the brain lesions caused by T. gondii inducing a Th2 immune response.
Keywords:Neurocysticercosis  Neurotoxoplasmosis  Co-infection  Immune reponse
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