Impact of Entamoeba histolytica on Lactase Activity and Intestinal Inflammation in Experimental Infected Mice

Document Type : Original Article

Authors

1 Departmet of Medical Parasitology, Faculty of Medicine, Cairo University, Cairo, Egypt.

2 Departmet of Biochemistry and Molecular Biology, Theodore Bilharz Research Institute, Egypt.

3 Departmet of Biochemistry and Molecular Biology, Faculty of medicine, Cairo university, Cairo, Egypt.

Abstract

Background and Objective: Lactose intolerance is one of the gastrointestinal disorders linked to Entamoeba histolytica, but the pathogenic factors that underlie this are still indistinct. This experimental study designed to determine the association between lactase enzyme activity and Entamoeba infection. Methodology: Forty mice were divided into 4 groups of 10 mice each that were used: uninfected mice (GI) (negative control); uninfected mice (GII) given lactose (positive control); Entamoeba histolytica-infected mice fed with lactose (GIII) and Entamoeba histolytica infected mice not receiving lactose (GIV). Entamoeba complex was identified by microscope and species differentiated molecularly. Lactase enzyme activity was assessed by spectrophotometry, and immunohistochemistry was used to examine and evaluate the expression of TNF-α and IL-1β in the intestine of each group. Results: Entamoeba complex cyst was detected microscopically, 10 selected samples were characterized and identified by molecular assay. E. histolytica was detected in 60% followed by E. moshkovski (30%) and E. dispar (1/10; 10%). Infected mice showed a significant decrease in lactase enzyme activity. The levels of TNF-α and IL-1β were elevated compared to mice that were non-infected (P<0.001). Conclusion: This study exposes a significant correlation between Entamoeba histolytica infection and decreased lactase enzyme activity, suggesting that parasitic invasion contributes to secondary lactose intolerance. The elevated intestinal expression of proinflammatory cytokines TNF-α and IL-1β in infected mice indicates that inflammation may play a crucial role in disrupting lactase function. Additional research is needed to explore the specific molecular pathways convoluted and to evaluate potential therapeutic interventions directing inflammation-mediated enzyme disruption in parasitic infections.

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