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. 1. Introduction Entamoeba histolytica is an enteric parasite that colonizes the human intestinal lumen and has the capacity to invade the epithelium. Although 90% of amebic infections are asymptomatic and self-limiting, there are an estimated 50 million cases of invasive infection annually [1, 2]. According to the WHO, Entamoeba histolytica is ranked third as a cause of death among parasites with 100,000 estimated deaths annually [1]. The morbidity and mortality of this parasite is primarily seen in developing countries. Ingestion of contaminated food or water containing infectious cysts leads to excystation in the intestine. 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]. The process of invasion and hepatic abscess formation has no apparent advantage for Entamoeba histolytica [3]. The logical question would then be why did this organism evolve to be a pathogen and not a commensal like its noninvasive cousin, Entamoeba dispar? One theory of Entamoeba histolytica’s origin of virulence is coincidental evolution. Host cells may have recognition patterns similar to those of enteric bacteria that the parasite has evolved to identify. Entamoeba histolytica has been shown to preferentially phagocytose cells coated with collectins, C-type lectins involved in recognition of ligands that are common to both bacteria and apoptotic cells [4]. An effective hijacking of the host’s own innate immune system to increase phagocytosis may have led to an invasive phenotype. In further support of this theory, Ghosh and Samuelson [3] have shown that several signaling proteins required for Entamoeba histolytica’s virulence are also 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]. Directed apoptosis and subsequent phagocytosis may serve to limit host
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