Entamoeba histolytica-Gut Microbiota Interaction: More Than Meets the Eye

Abstract

Amebiasis is a disease caused by the unicellular parasite Entamoeba histolytica. In most cases, the infection is asymptomatic but when symptomatic, the infection can cause dysentery and invasive extraintestinal complications. In the gut, E. histolytica feeds on bacteria. Increasing evidences support the role of the gut microbiota in the development of the disease. In this review we will discuss the consequences of E. histolytica infection on the gut microbiota. We will also discuss new evidences about the role of gut microbiota in regulating the resistance of the parasite to oxidative stress and its virulence.

Keywords: entamoeba histolytica; gut microbiota; resistance to nitrosative stress; resistance to oxidative stress; virulence.

Figure 1

Queuine produced by the gut microbiota regulates E. histolytica resistance to oxidative stress (OS) and virulence. 1. Queuine which is produced in the human gut by the microbiota and released upon lysis of the bacteria can be salvaged by E. histolytica. The mechanism used to uptake queuine is unknown. 2. Queuosine-modified tRNAs present inside bacteria can enter inside the parasite following their phagocytosis. The parasite may rely on a dedicated enzymatic machinery to salvage Q. One possible candidate for this function is DUF2419 (EHI_098190), an E. histolytica protein with structural similarity with DNA glycosidases. Work is in progress to characterize the involvement of EhDUF2419 in the salvage of Q from bacteria. 3. Queuine regulates the transcriptome of the parasite by upregulating the expression of genes involved in the resistance to OS and by downregulating the expression of genes involved in virulence [66]. 4. Protein synthesis is impaired in the parasite exposed to OS [66]. In presence of queuine, OS does not block protein synthesis. This mechanism may help the parasite to stand OS. 5. Queuosine-modified tRNAs are hypermethylated by Ehmeth, the amebic homolog of mammalian Dnmt2 [66]. Hypermethylation of tRNA^Asp_GUC has been correlated with the resistance of the parasite to OS and nitrosative stress (NS) [71,72]. It is possible that regulatory mechanisms described in 3 and 5 are linked [66]. This document has be created with BioRender.com (accessed on 10 March 2021).