Discerning the Molecular Mechanisms of Erythrophagocytosis in Entamoeba histolytica

Topics: Entamoeba histolytica, Protein, Cell membrane Pages: 12 (2174 words) Published: April 15, 2014

Discerning the Molecular Mechanisms of Entamoeba histolytica Erythrophagocytosis

Entamoeba histolytica is a protozoan parasite representing a serious public health care crisis worldwide. It primarily affects people in low-income regions of impoverished nations and may affect the colon, liver, spleen, lungs, and brain. Erythrophagocytosis is a process that is vital to the pathogenicity of E. histolytica and therefore, the examination of molecular mechanisms involved in this pathogenicity is crucial. Various groups of molecules are involved in erythrophagocytosis in E. histolytica including groups of actins, myosins, small GTPases, transmembrane proteins, and lectins. Due to the innate complexity of E. histolytica, further study is necessary to determine novel molecular mechanisms and work towards enacting public health solutions to E. histolytica. Entamoeba histolytica: A Severe Public Health problem

Entamoeba histolytica is a pathogenic protozoan parasite affecting primarily the colon and by extension, the liver. On some occasions the lungs, brain, and spleen may be infected as well, but this is not due to direct infection by Entamoeba but by secondary infection through close proximity to direct Entamoeba ulceration. Amebiasis is the clinical manifestation of symptomatic Entamoeba histolytica infection and affects approximately 50 million people worldwide, making it one of the more severe parasitic infections. Clinical symptoms of amebiasis include, but are not limited to: dysentery, weight loss, abdominal pain and cramping, fatigue, dehydration, and systemic bacteremia due to colic ulceration. Infection by Entamoeba histolytica can result in severe medical complications and requires prompt diagnosis and treatment with an amebicide followed by a luminal agent (to treat secondary bacterial infection due to ulceration).

The translation of “histolytica” into English literally means “tissue-destroying”, an apt moniker indeed; the pathogenicity of Entamoeba is innately linked to its ability to penetrate into the mucosal crypts of the colic lumen and this is, in turn, dependent on its ability to phagocytize erythrocytes, which for the purpose of this review is defined as the overall process of recognition, attachment, and endocytosis. For this reason, the understanding of the molecular mechanisms affecting phagocytosis by Entamoeba are vital in the development of novel treatments for Entamoeba histolytica, as well as being necessary to investigation of molecules that could result in public health solutions to Entamoeba-mediated amebiasis. Erythrophagocytosis in Entamoeba histolytica

Originally, it was thought (and by many today, still is), that visualization of phagocytized erythrocytes within an amoeba is exclusively indicative of Entamoeba histolytica infection. It is now known that this is not the case: virtually all species on Entamoeba phagocytize erythrocytes to some extent [1]. Despite this, Entamoeba histolytica’s efficiency in erythrophagocytosis does seem more pronounced [1] than other Entamoeba species, indicating a biochemical difference promoting either recognition, binding, or endocytosis of erythrocytes in E. histolytica as compared to other Entamoeba species. While not enough research has been conducted on these mechanisms to conclusively identify the factors that optimize erythrophagocytosis in E. histolytica as compared to other Entamoeba strains, studies have discovered molecules participating in the recognition, adhesion, and uptake of erythrocytes into E. histolytica cells. E. histolytica cells preferentially phagocytize apoptotic cells in which apoptosis is induced by the interaction of certain E. histolytica surface glycoproteins with various receptors found ubiquitously in human erythrocytes that then induce apoptosis mediated by the caspase groups of proteins as well as the calpain groups of proteins [2]. Molecular Mechanisms of Erythrocytic...

Cited: 1. Trissl, D, et. al. (1978) Surface Properties of Entamoeba histolytica: Increased rates of Human Erythrocyte Phagocytosis in Pathogenic Strains. J Exp. Med. 145, 1137-1143
3. Boettner, Douglas R. et al. (2005) Entamoeba histolytica and Entamoeba dispar Utilize Externalized Phosphatidylserine for Recognition and Phagocytosis of Erythrocytes. Infect. Immun. 73, 3422-3430
5. Aslam, Saima. et al. (2012). The Calmodulin-like Calcium Binding Protein EhCaBP3 of Entamoeba histolytica Regulates Phagocytosis and Is Involved in Actin Dynamics. Plos. Path. 8,  e1003055
7. McCoy, James J.; Mann, Barbara J. (2005) Proteomic analysis of Gal/GalNAc lectin-associated proteins in Entamoeba histolytica. Exp. Parasit. 110, 220-225
9. Voigt H. et al. (1999). Myosin IB from Entamoeba histolytica is involved in phagocytosis of human erythrocytes. J. Cell. Sci. 112, 1191-1201
11. Buss, Sarah N. et al. (2010) Members of the Entamoeba histolytica transmembrane kinase family play non-​redundant roles in growth and phagocytosis. Int. J. Parasit. 40, 833-433
13. Sateriale, Adam. et al. (2012) Feed-Forward Regulation of Phagocytosis by Entamoeba histolytica. Infect. Immun. 80, 4456-4462
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