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The benign helminth Hymenolepis diminuta ameliorates chemically induced colitis in a rat model system

Published online by Cambridge University Press:  18 June 2018

Kateřina Jirků Pomajbíková*
Affiliation:
Biology Centre, Czech Academy of Sciences, Institute of Parasitology, Branišovská 31, 370 05 České Budějovice, Czech Republic Department of Medical Biology, Faculty of Science, University of South-Bohemia, Branišovská 31, 370 05 České Budějovice, Czech Republic
Milan Jirků
Affiliation:
Biology Centre, Czech Academy of Sciences, Institute of Parasitology, Branišovská 31, 370 05 České Budějovice, Czech Republic
Jana Levá
Affiliation:
Biology Centre, Czech Academy of Sciences, Institute of Parasitology, Branišovská 31, 370 05 České Budějovice, Czech Republic Department of Medical Biology, Faculty of Science, University of South-Bohemia, Branišovská 31, 370 05 České Budějovice, Czech Republic
Kateřina Sobotková
Affiliation:
Biology Centre, Czech Academy of Sciences, Institute of Parasitology, Branišovská 31, 370 05 České Budějovice, Czech Republic
Evan Morien
Affiliation:
Department of Botany, Biodiversity Research Centre, University of British Columbia, 3200-6270 University Boulevard BC V6T 1Z4, Vancouver, Canada
Laura Wegener Parfrey*
Affiliation:
Department of Botany, Biodiversity Research Centre, University of British Columbia, 3200-6270 University Boulevard BC V6T 1Z4, Vancouver, Canada Department of Zoology, University of British Columbia, 4200-6270 University Boulevard BC V6T 1Z4, Vancouver, Canada
*
Author for correspondence: Laura Wegener Parfrey, Kateřina Jirků Pomajbíková, E-mail: lwparfrey@botany.ubc.ca, pomajbikova@paru.cas.cz
Author for correspondence: Laura Wegener Parfrey, Kateřina Jirků Pomajbíková, E-mail: lwparfrey@botany.ubc.ca, pomajbikova@paru.cas.cz

Abstract

The tapeworm Hymenolepis diminuta is a model for the impact of helminth colonization on the mammalian immune system and a candidate therapeutic agent for immune mediated inflammatory diseases (IMIDs). In mice, H. diminuta protects against models of inflammatory colitis by inducing a strong type 2 immune response that is activated to expel the immature worm. Rats are the definitive host of H. diminuta, and are colonized stably and over long time periods without harming the host. Rats mount a mild type 2 immune response to H. diminuta colonization, but this response does not generally ameliorate colitis. Here we investigate the ability of different life cycle stages of H. diminuta to protect rats against a model of colitis induced through application of the haptenizing agent dinitrobenzene sulphonic acid (DNBS) directly to the colon, and monitor rat clinical health, systemic inflammation measured by TNFα and IL-1β, and the gut microbiota. We show that immature H. diminuta induces a type 2 response as measured by increased IL-4, IL-13 and IL-10 expression, but does not protect against colitis. In contrast, rats colonized with mature H. diminuta and challenged with severe colitis (two applications of DNBS) have lower inflammation and less severe clinical symptoms. This effect is not related the initial type 2 immune response. The gut microbiota is disrupted during colitis and does not appear to play an overt role in H. diminuta-mediated protection.

Type
Special Issue Research Article
Copyright
Copyright © Cambridge University Press 2018 

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