Abstract
The protozoan parasite Entamoeba histolytica is responsible for invasive intestinal and extraintestinal amebiasis. The virulence of Entamoeba histolytica is strongly correlated with the parasite's capacity to effectively kill and phagocytose host cells. The process by which host cells are killed and phagocytosed follows a sequential model of adherence, cell killing, initiation of phagocytosis, and engulfment. This paper presents recent advances in the cytolytic and phagocytic processes of Entamoeba histolytica in context of the sequential model.
Highlights
Entamoeba histolytica is an enteric parasite that colonizes the human intestinal lumen and has the capacity to invade the epithelium
Tetracycline-regulated expression of a truncated intracellular domain of the GalNAc lectin heavy subunit has been shown to significantly decrease adherence to host cells in vitro [24]. These data suggest that the lectin participates in outside-to-inside signaling, which is likely through the β2 integrin homologous intracellular domain of the GalNAc heavy subunit
These functions in adhesion and signaling place the GalNAc lectin firmly at the nexus of virulence, though there are other Entamoeba histolytica proteins that have been implicated in adherence
Summary
Entamoeba histolytica is an enteric parasite that colonizes the human intestinal lumen and has the capacity to invade the epithelium. Each cyst produces eight motile trophozoites, which colonize the host’s colon In those cases where the infection is not self limiting, amebic dysentery and liver abscess formation can occur [2]. Host cells may have recognition patterns similar to those of enteric bacteria that the parasite has evolved to identify. In further support of this theory, Ghosh and Samuelson [3] have shown that several signaling proteins required for Entamoeba histolytica’s virulence are utilized to kill and phagocytose bacteria. Another seemingly plausible explanation is that Entamoeba histolytica’s invasive phenotype arose in response to host defense mechanisms [5]. For the purpose of this review, cell killing and phagocytosis have been organized in a sequential model involving (i) adherence to the host cell surface, (ii) contact-dependent cell killing, (iii) initiation of phagocytosis, and (iv) engulfment (see Figure 1)
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