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The Effect of Entamoeba histolytica on Muc2 Mucin and Intestinal Permeability

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Amebiasis

Abstract

The intestinal parasite Entamoeba histolytica (Eh) is a significant health risk in the developing world where infection occurs via ingestion of contaminated food or water. The resulting disease, amebiasis, claims 100,000 lives each year. In the colon, the parasite colonizes the mucous layer and interacts with the underlying mucosa to induce a variety of symptoms. The intestinal barrier has three main components: bacteria and host proteins found within the lumen, a protective layer of mucus, and a single layer of intestinal epithelial cells (IEC) connected by tight junctions (TJ). Eh possesses a variety of virulence components that target the intestinal barrier to cause increased gut permeability, resulting in diarrhea. In the colon Eh can phagocytose pathogenic bacteria, which may increase the virulence of the parasite. Moreover, Eh binds colonic mucins via the parasite surface Gal/GalNAc lectin to facilitate colonization of the mucous layer. Subsequently, the virulence factor, EhCP-A5, degrades the MUC2 polymer, allowing the parasite access to the epithelia where it binds to and destroys IEC by apoptosis or alters the expression of TJ proteins, causing secretory diarrhea. The sequence of events in intestinal amebiasis is not well understood and is based largely on in vitro and in vivo models of the disease.

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Acknowledgments

Research presented in this chapter was supported by grants from the Canadian Institute for Health Research (CIHR), Natural Science and Engineering Research Council of Canada, Crohn’s and Colitis Foundation of Canada (CCFC), and the Alberta Inflammatory Bowel Disease Consortium. V.K.S. and E.T. are supported by Alberta Innovates Health Solutions Studentships. K.C. holds a Tier 1 Canada Research Chair supported by CIHR.

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Kissoon-Singh, V., Trusevych, E., Chadee, K. (2015). The Effect of Entamoeba histolytica on Muc2 Mucin and Intestinal Permeability. In: Nozaki, T., Bhattacharya, A. (eds) Amebiasis. Springer, Tokyo. https://doi.org/10.1007/978-4-431-55200-0_27

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