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

Abstract

SummaryThe tumour‐like growth of larval Echinococcus multilocularis 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 E. multilocularis infection on murine dextran sodium sulphate (DSS) ‐induced colitis. At 3 months after E. multilocularis 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 E. multilocularis infection, which correlated with down‐regulation of T helper type 1 (Th1)/Th17 T‐cell responses in the colon tissue. Echinococcus multilocularis 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, E. multilocularis infection remarkably reduces DSS‐induced colitis in mice by attenuating Th1/Th17‐mediated immune reactions.

Schistosoma japonicum peptide SJMHE1 inhibits acute and chronic colitis induced by dextran sulfate sodium in mice

“…The pathogenesis of CD and UC is usually considered to be different, with CD is dominated by IFN-γ and IL-17A from Th1 and Th17 cells, respectively, and UC mediated by IL-4 and IL-13 from Th2 cells [ 1 ]. Consistent with the findings in mice with DSS-induced acute colitis [ 31 – 33 ], the expression of IL-17 mRNA in the splenocytes and of IFN-γ and IL-17 mRNA in the colon increased in the DSS and/or DSS/PBS groups. However, SJMHE1 treatment reduced the expression levels of IFN-γ and IL-17 mRNA, increased the expression levels of IL-4, TGF-β and IL-35 mRNA in the splenocytes and increased the expression levels of IL-4, IL-10, TGF-β and IL-35 mRNA in the colon of mice.…”

Immune Protection of a Helminth Protein in the DSS-Induced Colitis Model in Mice

“…The regulation of parasite-specific immune response affects not only helminth antigens, but also unrelated antigens. In recent years, clinical and experimental evidence has demonstrated that infection with parasitic helminth protects hosts from IBD; for example, a case control study in South Africa demonstrated protective association of childhood helminth infection against the development of IBD ( 10 ) ; pre-existing helminth Echinococcus multilocularis ( 11 ), Heligmosomoides polygyrus ( 12 ), or Hymenolepis diminuta ( 13 ), etc., infection have been shown to reduce chemically-induced colitis in mice by modulating the immune responses of their hosts.…”

Schistosoma Japonicum Peptide SJMHE1 Inhibits Acute And Chronic Colitis Induced By Dextran Sulphate Sodium In Mice

“…CD is dominated by IFN-γ and IL-17A from Th1 and Th17 cells, respectively, whereas UC is mediated by IL-4 and IL-13 from Th2 cells [1]. Consistent with the ndings in mice with DSS-induced acute colitis [29,30,31], the mRNA expression of IL-17 in the splenocytes and the mRNA expression of IFN-γ and IL-17 in the colon increased in the DSS and DSS/PBS groups. However, SJMHE1 treatment reduced the mRNA expression levels of IFN-γ and IL-17, increased the mRNA expression levels of IL-4 and TGF-β in the splenocytes, and increased the mRNA expression levels of IL-4, IL-10, TGF-β, and IL-35 in the colon of mice.…”