Nascimento BB1,
Cartelle CT1,
Noviello ML1,
Pinheiro BV2,
de Almeida Vitor RW2,
Souza DDG3,
de Vasconcelos Generoso S4,
Cardoso VN4,
Martins FDS3,
Nicoli JR3,
Arantes RME1.
Abstract
Toxoplasmosis represents one of the most common zoonosis worldwide. Its agent, Toxoplasma gondii, causes a severe innate pro-inflammatory response. The indigenous intestinal microbiota promotes host animal homoeostasis and may protect the host against pathogens. Germ-free (GF) animals provide an important tool for the study of interactions between host and microbiota. In this study, we assessed the role of indigenous microorganisms in disease development utilizing a murine toxoplasmosis model, which includes conventional (CV) and GF NIH Swiss mice. CV and GF mice orally inoculated with T. gondii had similar survival curves. However, disease developed differently in the two animal groups. In CV mice, intestinal permeability increased and levels of intestinal pro-inflammatory cytokines were altered. In GF animals, there were discrete epithelial degenerative changes and mucosal oedema, but the liver and lungs displayed significant lesions. We conclude that, despite similar survival curves, CV animals succumb to an exaggerated inflammatory response, whereas GF mice fail to produce an adequate systemic response.
© 2017 The Authors. International Journal of Experimental Pathology © 2017 International Journal of Experimental Pathology.
KEYWORDS:
Toxoplasma gondii ; germ-free mice; gut inflammation; microbiota; toxoplasmosis
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