4.7 Article

Intestinal microbiota regulates colonic inflammation in fluorosis mice by TLR/NF-κB pathway through short-chain fatty acids

Journal

FOOD AND CHEMICAL TOXICOLOGY
Volume 178, Issue -, Pages -

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2023.113866

Keywords

Fluoride; Pesuo germ-free mice; FMT; SCFAs; Dysbiosis; Toll -like receptors

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In this study, it was found that both intestinal inflammation and microbial dysbiosis were present in patients with fluorosis. The research suggests that the development of colonic inflammation may be more directly influenced by microbial disorders rather than fluoride exposure. Fecal microbiota transplantation and supplementation of short-chain fatty acids were found to alleviate colonic inflammation in fluoride-exposed mice by regulating the TLR/NF-κB pathway.
Intestinal inflammation and microbial dysbiosis are found simultaneously in patients with fluorosis. However, whether the inflammation derived from fluoride exposure only or intestinal microbial disorders has not been clarified. In this study, 100 mg/L NaF exposure for 90 days significantly elevated the expressions of inflammatory factors (TNF-& alpha;, IL-1 & beta;, IL-6, IFN-& gamma;, TGF-& beta;, and IL-10), and the levels of TLR4, TRAF6, Myd88, IKK & beta;, and NF-& kappa;B P65 in mouse colon, while the above factors were reduced in pseudo germ-free mice with fluorosis, hinting that disordered microbiota might play a more direct role in the development of colonic inflammation than fluoride. Fecal microbiota transplantation (FMT) lowered the levels of inflammatory factors and inactivated the TLR/NF & kappa;B pathway in fluoride-exposed mice. In addition, supplementing short-chain fatty acids (SCFAs) exhibited the identical effects to the model of FMT. In summary, intestinal microbiota may alleviate the colonic inflammatory of mice with fluorosis by regulating TLR/NF-& kappa;B pathway through SCFAs.

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