Influence of indigenous microbiota on experimental toxoplasmosis in conventional and germ‐free mice

Summary Toxoplasmosis represents one of the most common zoonoses 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 provid...

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Published in:International journal of experimental pathology Vol. 98; no. 4; pp. 191 - 202
Main Authors: Nascimento, Bruna B., Cartelle, Christiane T., Noviello, Maria de L., Pinheiro, Breno V., Almeida Vitor, Ricardo W., Souza, Danielle da G., Vasconcelos Generoso, Simone, Cardoso, Valbert N., Martins, Flaviano dos S., Nicoli, Jacques R., Arantes, Rosa M. E.
Format: Journal Article
Language:English
Published: England Wiley Subscription Services, Inc 01-08-2017
John Wiley and Sons Inc
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Summary:Summary Toxoplasmosis represents one of the most common zoonoses 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.
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ISSN:0959-9673
1365-2613
DOI:10.1111/iep.12236