Fluoride Action Network



  • Fluoride inhibited the secretion of glycoproteins.
  • Fluoride induced relative number of goblet and mast cells down-regulate.
  • Fluoride inhibited epithelial cells proliferation.
  • Fluoride induced cecal epithelial barrier damages.
  • Fluoride interfered the composition of intestinal microflora.

Intestinal microflora play an important role in maintaining the homeostasis of the intestinal microenvironment, but fluoride-induced changes in intestinal mechanical barrier and intestinal microflora have not been well studied. Given this paucity of information, this study aims to determine the effects of high fluoride level on intestinal mechanical barrier and intestinal microflora in the cecum of mice. Seventy-two female 21-day-old Kunming mice were randomly assigned to three groups and raised for 70 days. Changes in intestinal pathomorphology and intestinal epithelial cell proliferation were observed by haematoxylin and eosin-staining and Brdu measurement, respectively. The distribution of goblet cells, glycoproteins and mast cells was analysed through Alcian blue and periodic acid-Schiff (AB-PAS) staining, Periodic Acid-Schiff (PAS) staining, and toluidine blue staining. Results showed that excessive fluoride damaged the structure of the cecal tissues, inhibited epithelial cell proliferation and decreased the relative distribution of goblet cells, glycoproteins and mast cells that are involved in defense responses. Intestinal microflora sequencing analysis revealed that the composition of the diversity and composition of intestinal microflora was altered by excessive fluoride based on 16S rRNA amplicon sequencing. The relative abundance of Firmicutes (P?=?0.03174), Bacteroidetes (P?=?0.04462), Actinobacteria (P?=?0.01085) and Spirochacteria (P?=?0.04084) was significantly changed in the fluoride group as compared with the control group. In conclusion, excessive fluoride intake induced intestinal barrier damage, leading to changes in cecal composition, epithelium secretion and intestinal microflora.