Echinostoma caproni (Trematoda): differential in vivo mucin expression and glycosylation in high‐ and low‐compatible hosts. (January 2015)

• Record Type: Journal Article
• Authors: Cortés, A.; Muñoz‐Antoli, C.; Sotillo, J.; Fried, B.; Esteban, J. G.; Toledo, R.
• Is Part Of: Parasite immunology. Volume 37:Number 1(2015:Jan.)
• Page Start: 32
• Page End: 42
• Publication Date: 2015-01
• Subjects: Veterinary parasitology -- Immunological aspects -- Periodicals; Host-parasite relationships -- Immunological aspects -- Periodicals; 571.96
• DOI: 10.1111/pim.12159
• Languages: English
• ISSNs: 0141-9838

Abstract

<abstract abstract-type="main" id="pim12159-abs-0001"> <title>Summary</title> <p>Enhanced mucus production and release appears to be a common mechanism for the clearance of intestinal helminths, and this expulsion is normally mediated by Th2‐type immune responses. To investigate the factors determining the expulsion of intestinal helminths, we have analysed <italic>in vivo</italic> expression of mucin genes at the site of infection in two host species displaying different compatibility with <italic>Echinostoma caproni</italic> (Trematoda). Surprisingly, a general down‐regulation on mucin mRNA expression was detected in low‐compatible hosts (rats) coinciding with the development of Th2/Th17 responses and the early rejection of the worms from the intestinal lumen. This suggests the existence of a mechanism by which the parasites can modulate the mucus barrier to favour their survival. In highly compatible hosts (mice), some mucin genes were found to be up‐regulated throughout the infection, probably, to protect the intestinal epithelium against the infection‐induced inflammation developed in this host species. Moreover, infection‐induced changes on mucin glycans were also studied by lectin histochemistry. Similar alterations were detected in the ileum of infected mice and rats, except with SNA lectin, indicating that sylated mucins might play an important role in determining the evolution of the infection in each host species.</p> </abstract>