Little is known regarding the signals that initiate an acute inflammatory response to Entamoeba histolytica during liver abscess development in the hamster model. Inflammation is the local response to cellular injury, during this process arachidonic acid is released from cell membranes and is metabolised into a number of substances collectively referred as eicosanoids. Among them, prostaglandins are important mediators that participate as potent effectors on immune cells influencing the adaptive immune response mediated by T cell sub-populations. In this paper we will review the participation of PGE2 in amoebic liver abscess development through the induction of COX-2 expression by neutrophils and macrophages, together with the induction of a COX-like activity expression by e. histolytica trophozoites. Additionally, the participation of signalling through TLRs and the participation of pro-inflammatory cytokines in early stages of the abscess development will be described. Finally, we will discuss how all these factors are utilised by E. histolytica to promote inflammation as a pathogenesis mechanism.
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