Larval <italic>Echinococcus multilocularis</italic> infection reduces dextran sulphate sodium‐induced colitis in mice by attenuating T helper type 1/type 17‐mediated immune reactions.

Summary: The tumour‐like growth of larval <italic>Echinococcus multilocularis</italic> tissue (causing alveolar echinococcosis, AE) is directly linked to the nature/orientation of the periparasitic host immune‐mediated processes. Parasite‐mediated immune suppression is a hallmark triggering infection outcome in both chronic human and murine AE. So far, little is known about secondary systemic immune effects of this pathogen on other concomitant diseases, e.g. endogenous gut inflammation. We examined the influence of <italic>E. multilocularis</italic> infection on murine dextran sodium sulphate (DSS) ‐induced colitis. At 3 months after <italic>E. multilocularis</italic> infection (chronic stage), the mice were challenged with 3% DSS in the drinking water for 5 days plus subsequently with tap water (alone) for another 4 days. After necropsy, fixed tissues/organs were sectioned and stained with haematoxylin & eosin for assessing inflammatory reactions. Cytokine levels were measured by flow cytometry and quantitative RT‐PCR. Colitis severity was assessed (by board‐certified veterinary pathologists) regarding (i) colon length, (ii) weight loss and (iii) a semi‐quantitative score of morphological changes. The histopathological analysis of the colon showed a significant reduction of DSS‐induced gut inflammation by concomitant <italic>E. multilocularis</italic> infection, which correlated with down‐regulation of T helper type 1 (Th1)/Th17 T‐cell responses in the colon tissue. <italic>Echinococcus multilocularis</italic> infection markedly reduced the severity of DSS‐induced gut inflammation upon down‐regulation of Th1/Th17 cytokine expression and attenuation of CD11b⁺ cell activation. In conclusion, <italic>E. multilocularis</italic> infection remarkably reduces DSS‐induced colitis in mice by attenuating Th1/Th17‐mediated immune reactions. [ABSTRACT FROM AUTHOR]