High cellulose diet promotes intestinal motility through regulating intestinal immune homeostasis and serotonin biosynthesis.

It is widely accepted dietary fiber intimately linked to inflammatory and nervous diseases, which often been described with altered gastrointestinal (GI) motility. However, how dose dietary fiber modulate inflammation and crosstalk influence GI function has not been explained in detail. We found fiber-free diet reduced intestinal motility, accompanied by upregulated proinflammatory immunocytes and inflammatory cytokines in colon of mice. We also discovered high-cellulose diet increased synthesis of serotonin and expression of neurotrophic factors, both of that have been reported involved in promoting intestinal motility. In addition, metabolomics analysis showed increased tryptophan metabolites in high-cellulose diet mice, which happened to be required for serotonin biosynthesis. Further analysis revealed high-cellulose diet changed the composition of gut microbiota, in particular by altering the ratio of Firmicutes to Bacteroidetes, consequently, concentration of short-chain fatty acids (SCFAs), especially acetate. Orally administration of acetate confirmed its modulating to serotonin synthesis, neurotrophic factors expression and immunocyte differentiation through regulating histone deacetylase (HDAC3) activity in colon. Together, our results demonstrated high-cellulose diet promote intestinal motility through regulating intestinal homeostasis and enteric nervous system by increasing acetate production and HDAC3 inhibition. Thus, rich cellulose diet or acetate supplement can be considered as dietary advice to improve clinically intestinal motility insufficiency.

[Gut mobility attenuation induced by antibiotics is associated with overactivation of enteric glial cells in mice].

Objective To explore the relationship between gut motility and enteric glial cell activation in antibiotics-treated mice. Methods We got the mice with lower intestinal flora through antibiotics (ABX) cocktails treatment, and compared gut mobility between ABX mice and control mice by detecting the time of carmine red going through gastrointestinal tract and the fecal pellets in the same time. Immunofluorescence histochemistry was used to detect the distribution of enteric glial cells and neurons in myenteric nerve plexus of the two groups of mice. Real-time fluorescence quantitative PCR was used to detect the mRNA levels of glial fibrillary acidic protein (GFAP), glial cell-derived neurotrophic factor (GDNF), S100B and nerve growth factor (NGF), which were related to enteric glial cell activation and function both in colon and ileum. The population of regulatory T cells (Tregs) and Th17 cells in intestinal lamina propria was assessed by flow cytometry. Results Antibiotics treatment induced a significant reduction of intestinal flora in the mice, which was accompanied by cecum volume expansion, colon shortening and gut motility attenuation. In addition, mRNA levels of GFAP, GDNF, S100B, and NGF in colon of ABX mouse gastrointestinal tract increased, while the population of Tregs and Th17 cells in colonic lamina propria decreased. Conclusion The attenuation of gut motility induced by antibiotics treatment may be related to the excessive activation of enteric glial cells. However, the activation of enteric glial cells after antibiotics treatment is not related to intestinal inflammation.