Abstract
Mouse strain-specific differences in the carbohydrate composition of intestinal mucins were hypothesized to account for strain-dependent susceptibility to Entamoeba histolytica. To test this hypothesis, intestinal mucins from susceptible and resistant inbred strains of mice were analyzed for their O-glycan content and for their ability to inhibit amoebic adherence to (GalNAc)12–27-HSA neo-glycoproteins. The results showed that the colorectal mucin O-glycan of susceptible CBA mice was lower in sialic acid content than that of resistant C57BL/6 and BALB/c mice. Mucins from CBA mice were more potent inhibitors of E. histolytica adherence to neo-glycoproteins than were mucins from C57BL/6 or BALB/c mice. Consistent with the role of terminal Gal/GalNAc as a receptor for amoebic adherence, sialidase treatment of C57BL/6 and BALB/c colorectal mucins increased their ability to inhibit E. histolytica adherence to the neo-glycoproteins. These results provide evidence of mouse strain-specific differences in the sialic acids content of mucin O-glycans. These dissimilarities likely contribute to the differential susceptibility of the three mouse strains to E. histolytica infection.
Highlights
The anaerobic parasitic protozoan Entamoeba histolytica (E. histolytica) is estimated to infect about 1% of the world’s population, resulting in 40,000–100,000 deaths annually
The results showed that the affinity of E. histolytica toward mouse mucins is determined by the relative abundance of sialic acids on their O-glycans and that differences in sialic acid content may contribute to host susceptibility to the parasite
The most important finding of this work was the differences in the sialic acids content of large intestinal mucins among the three strains of mice tested, as it can, at least in part, explain the observed differential susceptibilities to E. histolytica infection
Summary
The anaerobic parasitic protozoan Entamoeba histolytica (E. histolytica) is estimated to infect about 1% of the world’s population (about 50 million people), resulting in 40,000–100,000 deaths annually. There, excystment results in the release of trophozoites, migration to the large intestine, and colonization by adherence to the mucous layer. Attachment of the parasite to the intestinal wall requires galactose (Gal)/N-acetylgalactosamine (GalNAc) inhibitable lectins, their heavy subunits (Hgls), which have been shown to bind the Gal and GalNAc residues exposed on the luminal surface of host mucins [1,2].
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