Effect of trimethylamine N-oxide on inflammation and the gut microbiota in Helicobacter pylori-infected mice.

• TMAO enhanced the viability and virulence of H. pylori in vitro. • TMAO facilitated the production of inflammatory factors induced by H. pylori. • TMAO increased the abundance of Escherichia_Shigella of H. pylori -infected mice. • TMAO may aggravate inflammation in association with the gut microbiota of mice. Diet is one of the factors contributing to symptom of Helicobacter pylori (H. pylori) infection. Trimethylamine N-oxide (TMAO), a diet-related microbial metabolite, is associated with inflammatory and metabolic diseases. The aim of this study is to investigate the effects of TMAO intake on inflammation and gut microbiota composition in H. pylori -infected mice via 16S rRNA sequencing and biochemical analyses. The in vitro experiments showed that TMAO not only increased the expression of growth- and metabolism-associated genes and the urease activity of H. pylori , but increased the production of virulence factors. Moreover, TMAO intake increased the production of inflammatory markers and reduced the richness and diversity of the gut microbiota in H. pylori -infected mice. Further analysis showed that TMAO increased the relative abundance of Escherichia_Shigella in H. pylori -infected mice, which had positive correlation with the levels of LPS, CRP, and CXCL1. Collectively, our results suggest that TMAO may aggravate H. pylori -induced inflammation by increasing the viability and virulence of H. pylori and may aggravate inflammation in association with the gut microbiota in H. pylori -infected mice. This study may provide a novel insight into the mechanism for the effect of diet-derived metabolites such as TMAO on H. pylori -induced disease development. [ABSTRACT FROM AUTHOR]