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The host and parasite factors that influence susceptibility toEntamoeba histolyticainfection and disease are not well understood.Entamoeba histolyticapathogenicity has been considered by focusing principally on parasite rather than host factors. Thus, research has concentrated on explaining the molecular differences between pathogenicE. histolyticaand non-pathogenicE. dispar. However, the amoeba molecules considered most important for host tissue destruction (amoebapore, galactose/N-acetyl galactosamine inhibitable lectin, and cysteine proteinases) are present in both pathogenicE. histolytica andnon-pathogenicE. dispar. In addition, the genetic differences in pathogenicity amongE. histolyticaisolates are unlikely to completely explain the different outcomes of infection. Considering that the principal difference between pathogenic and non-pathogenic amoebas lies in their surface coats, we propose that pathogenicity of the amoebas is related to the composition and properties of the surface coat components (or pathogen-associated molecular patterns, PAMPs), and the ability of innate immune response to recognize these components and eliminate the parasite. According to this hypothesis, a key feature that may distinguish pathogenic (E. histolytica)from non-pathogenic(E. dispar)strains is whether or not they can overcome innate immune defences. A corollary of this hypothesis is that in susceptible individuals the PAMPs are either not recognized or they are recognized by a set of Toll-like receptors (TLRs) that leads to an inflammatory response. In both cases, the result is tissue damage. On the contrary, in resistant individuals the innate/inflammatory response, induced through the activation of a different set of TLRs, eliminates the parasite. [ABSTRACT FROM AUTHOR]

Background: The aim of the present study was to determine if the inflammation and/or immunosuppression induced by Entamoeba histolytica may contribute to amebic invasion., Material/methods: Dexamethasone was administered three days before and three days after inoculation of hamsters with E. histolytica. Seven days alter inoculation the animals were sacrificed and the sizes of their amebic liver abscesses were determined. The number of neutrophils, macrophages, T and B cells in the peritoneum as well as the production of nitric oxide and the susceptibility to Listeria monocytogenes infection was also determined., Results: Dexamethasone treatment significantly reduced the number of T lymphocytes in thymus and spleen. The number of neutrophils, macrophages and T lymphocytes in the peritoneal exudate was also reduced as well as the production of nitric oxide and the microbicidal activity against Listeria monocytogenes. However, in the animals treated with a high dose of dexamethasone the size of the liver abscesses was significantly smaller than in the untreated animals., Conclusions: The results suggest that macrophage and T cell-mediated immunity is not relevant as a protective mechanism because tissue invasion by E. histolytica was reduced in immunosuppresed animals. On the contrary, the inflammatory process may contribute to the invasion and liver damage.