Aspartame enhances the scavenging activity of mice tolow-dose Escherichia coli infection via strengthening macrophage phagocytosis caused by sweet taste receptor activation.

Abstract

Aspartame is the most common artificial sweetener and a famous sweet-taste receptor agonist. Macrophages are essential in the antibacterial system to maintain the stability of the intestinal environment. Recently, the sweet taste receptor has been found in macrophages. However, the effects of aspartame on macrophage phagocytosis in the gastrointestinal tract are little known. The current study sought to assess the influence of aspartame intake on the scavenging activity of mice to low-dose Escherichia coli infection and related mechanisms. Firstly, no inflammatory response or pathological injury was observed in the intestines of mice after oral administration of aspartame (25-100 mg/kg, i.g.) for 2 weeks. Subsequently, aspartame intake was found to enhance the scavenging activity of mice to low-dose E. coli infection. Similarly, aspartame dose-dependent strengthened the ability of RAW264.7 cells to phagocytose GFP-E.coli J96. Further mechanism evaluation reflected that aspartame could enhance macrophage phagocytosis, migration, and rearrangement via PLCβ-2/Ca2+/PKCβ/Rho A/ROCK1 pathway caused by sweet taste receptor activation. In conclusion, the present study, for the first time, demonstrated that aspartame could enhance the scavenging activity of mice to low-dose E. coli infection via strengthening macrophage phagocytic function through activating sweet taste receptor. It is then suggested that aspartame may affect the antibacterial activity of human gastrointestinal macrophages, and further studies need to validate these effects.