Effects of sodium butyrate supplementation on inflammation, gut microbiota, and short-chain fatty acids in Helicobacter pylori-infected mice.

Abstract

Inflammation induced by Helicobacter pylori (H.pylori) infection is the basis for the pathogenesis of H.pylori. Butyric acid, a diet-related microbial-associated metabolite, is connected to inflammation, metabolic syndrome, and other diseases. Several studies have indicated the effects of sodium butyrate (SB) against bacteria; however, the effects of SB on the main virulence factors of H.pylori, H.pylori-induced inflammation, and gut microbiota composition remain unclear. SB was supplemented in H.pylori coculture and administered to mice infected with H.pylori. The effects of SB intake on inflammation, gut microbiota composition, and short-chain fatty acids (SCFAs) in H.pylori-infected mice were assessed. The in vitro experiments demonstrated that SB not only inhibited the growth of H.pylori but also decreased the mRNA expression of CagA and VacA. SB intake reduced the production of virulence factors in H.pylori-infected mice, inhibited the IκBα/NF-κB pathway by reducing the expression of Toll-like receptors (TLRs), and reduced the production of TNF-α and IL-8. Further analysis demonstrated that H.pylori infection altered the relative abundance of the intestinal microbial community in mice. The level of SCFAs in the feces of H.pylori-infected mice was changed, although the intake of SB did not obviously change the level of SCFAs. Our study showed that SB may decrease H.pylori-induced inflammation by inhibiting the viability and virulence of H.pylori and may reduce inflammation in association with the gut microbiota in H.pylori-infected mice. This study may provide novel insights into the mechanisms by which SB, a diet-related microbial-associated metabolite, affects H.pylori-induced disease development.