Figure 3.

The microbiota has a role to play in the lifecycle of E. histolytica and tissue responses. The balance between trophozoite and cyst is strongly influenced by the microbiota. First, amoebae phagocytose bacteria and derived nutrients promote the growth of trophozoites. Secreted bacterial products such as short-chain fatty acids (SCFAs) are expected to provide energy for parasite growth. During carbon source deprivation, SCFAs stimulate the production of mucin, which could be used as a carbon source. Acetate is a SCFA that induces encystation in vitro in E. histolytica. Second, an important activity of bacteria is to act as a parasite survival aid in stressful situations like oxidative stress (OS); it regulates the expression of amoebic genes, metabolites such as oxalacetate and queuine, derived from Enterobacteriaceae, protect E. histolytica from OS. This response is not universal since Lactobacillus acidophilus (a probiotic) modifies the amoebic transcriptome differently and causes oxidation of vital E. histolytica proteins leading to the death of trophozoites. Major lesions occurring at the early stages of contact between E. histolytica and the intestinal epithelium led to disruption of tight junctions combined with disruption of ion channels tissue architecture collapse. Mammalian cells die by trogocytosis, apoptosis and phagocytosis. The inflammatory response occurs leading to cell death, the microbiota influence alarmins activity. For references see the main text.