Fluoride Depletes Acidogenic Taxa in Oral but Not Gut Microbial Communities in Mice

Yasuda, Koji; Hsu, Tiffany Y.; Gallini, Carey Ann; Mclver, Lauren J.; Schwager, Emma; Shi, Andy; DuLong, Casey; Schwager, Randall; Abu-Ali, Galeb; Franzosa, Eric A.; Garrett, Wendy S.; Huttenhower, Curtis; Morgan, Xochitl C.

doi:10.1128/msystems.00047-17

Cited by 23 publications

(14 citation statements)

References 47 publications

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“…These fluoride-induced microbial changes were associated with histological gut abnormalities including evidence of a damaged epithelial barrier, decreased crypt depth, and lower epithelial cell proliferation, relative densities of goblet cells, glycoproteins, and intestinal mast cells (Liu et al 2019b). However, one study in mice found no significant shifts in gut microbial community composition with a lower dose and shorter duration of fluoride added to water (Yasuda et al 2017). Therefore, fluoride can alter the intestinal microbiota and gut health in ways that may influence blood glucose, but the dose and duration of fluoride are key factors to consider.…”

Section: Fluoridementioning

confidence: 99%

Micronutrients impact the gut microbiota and blood glucose

Barra

Anhê

Cavallari

et al. 2021

Journal of Endocrinology

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Micronutrients influence hormone action and host metabolism. Dietary minerals, trace elements and vitamins can alter blood glucose and cellular glucose metabolism and several micronutrients are associated with risk and progression of type 2 diabetes. Dietary components, microbes and host immune, endocrine, and metabolic responses all interact in the intestine. There has been a focus on macronutrients modifying the host-microbe relationship in metabolic disease. Micronutrients are positioned to alter host-microbe symbiosis that participates in host endocrine control of glucose metabolism. Minerals and trace elements can alter the composition of the intestinal microbiota, gut barrier function, compartmentalized metabolic inflammation, cellular glucose transport and endocrine control of glucose metabolism, including insulin and thyroid hormones. Dietary vitamins also influence the composition of the intestinal microbiota and vitamins can be biotransformed by gut microbes. Host-microbe regulation of vitamins can alter immunity, lipid and glucose metabolism, and cell fate and function of pancreatic beta cells. Causal effects of micronutrients in host-microbe metabolism are still emerging and the mechanisms linking dietary excess or deficiency of specific micronutrients to changes in gut microbes directly linked to metabolic disease risk are not yet clear. Dietary fiber, fat, protein, and carbohydrates are key dietary factors that impact how microbes participate in host glucose metabolism. It is possible that micronutrient and microbiota-derived factors also participate in host-microbe responses that tip the balance in endocrine control of host glucose metabolism. Dietary micronutrients should be considered, tested, and controlled in preclinical and clinical studies investigating host-microbe factors in metabolic diseases.

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Section: Fluoridementioning

confidence: 99%

Micronutrients impact the gut microbiota and blood glucose

Barra

Anhê

Cavallari

et al. 2021

Journal of Endocrinology

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“…Similarly, exposure to fluoride can induce the imbalance of microbiological composition. Yasuda et al (2017) found that fluoride exposure causes a depletion of acidogenic bacterial genera in oral community. Luo et al (2016) reported that excessive fluoride intake induces a reduction of Lactobacillus spp.…”

Section: Introductionmentioning

confidence: 99%

Lactobacillus johnsonii BS15 improves intestinal environment against fluoride-induced memory impairment in mice—a study based on the gut–brain axis hypothesis

Xin

Zeng

Wang

et al. 2020

PeerJ

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Background Excessive fluoride can lead to chronic neurodegeneration characterized by neuron and myelin loss and memory dysfunction. The gut–brain axis hypothesis suggests that gut microbiota plays a crucial role in regulating brain function. Thus, using probiotics to adjust the gut microenvironment may be a potential therapy for mental diseases. Methods Mice in the prob group were administrated with Lactobacillus johnsonii BS15 for 28 days prior to and throughout a 70-day exposure to sodium fluoride. The drinking water of all groups (F and prob groups) except the control group were replaced by high-fluoride water (100 mg NaF/L) on day 28. Animals in each group were divided into two subsets: one underwent behavioral test, and the other was sacrificed for sampling. The mRNA expression level and protein content related to inflammatory reaction in the ileum and hippocampus were respectively detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA). The mRNA expression levels of proteins related to myelin structure, apoptosis, and memory in the hippocampus and tight junction proteins in the ileum were determined by RT-qPCR and/or immunohistochemistry. Gut permeability markers (D-lactate and diamine oxidase (DAO)) in the serum were also examined by ELISA. Results The results showed that fluoride exposure induced a lower spontaneous exploration (P < 0.05) in T-maze test, which indicated an impairment of memory. Spontaneous exploration of BS15-treated mice was significantly higher (P < 0.05) than that in F group. Fluoride reduced (P < 0.05) levels of myelin structural protein (proteolipid protein) and neurogenesis-associated proteins (brain-derived neurotrophic factor and cAMP/Ca2+ responsive element-binding protein), induced disordered inflammatory cytokines (TNF-α, IFN-γ, and IL-6; P < 0.05), increased pro-apoptotic genes (caspase-3; P < 0.05), and decreased anti-apoptotic genes (Bcl-2; P < 0.05) in the hippocampus, of which the influences were reversed by BS15. BS15 treatment exerted significant preventive effects on reversing the gut inflammation induced by excessive fluoride intake by reducing (P < 0.05) the levels of pro-inflammatory cytokines (tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ)) and remarkably increasing (P < 0.05) the level of anti-inflammatory cytokines (IL-10). Moreover, the serum DAO activity and D-lactate concentration significantly increased by fluoride were also reduced (P < 0.05) by BS15. This result indicated the profitable effect of BS15 on gut permeability. Conclusion L. johnsonii BS15 intake could benefit the neuroinflammation and demyelination in the hippocampus by improving the gut environment and ameliorating fluorine-induced memory dysfunction.

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“…Interestingly, uoride failed to promote the proliferation of Erysipelotrichaceae in the absence of HFD, which might explain why uoride could not induce obesity in ND mice. In a similar work, uoride also showed limited effect on gut microbial communities in mice fed on standard mouse chow [57].…”

Section: Discussionmentioning

confidence: 73%

Fluoride Induced Leaky Gut and Bloom of Erysipelatoclostridium Ramosum Mediate the Exacerbation of Obesity in High-Fat-Diet Fed Mice

Chen

Peng

Huang

et al. 2021

Preprint

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Background: Fluoride, a necessary mineral element for our health, is widely presented in drinking water and foods. The intake of excessive fluoride showed potential risk to human health. A strong relation between fluoride exposure and obesity has been reported. However, the knowledge on the potential mechanisms on fluoride-induced obesity is still limited.Results: In this work, we showed here that fluoride alone did not induce obesity in normal diet fed mice, whereas, it could trigger exacerbation of obesity in high-fat diet (HFD) fed mice. Fluoride impaired intestinal barrier and activated Toll-like receptor 4 (TLR4) signaling to induce obesity, which was further verified in TLR4-/- mice. Furthermore, fluoride could deteriorate the gut microbiota in HFD mice. The fecal microbiota transplantation from fluoride-induced mice was sufficient to induce obesity, while the exacerbation of obesity by fluoride was blocked upon gut microbiota depletion. The fluoride-induced bloom of Erysipelatoclostridium ramosum belonged to Erysipelotrichaceae was responsible for exacerbation of obesity. In addition, a potential strategy for prevention of fluoride-induced obesity was proposed by intervention with polysaccharides from Fuzhuan brick tea.Conclusions: Overall, these results provide the first evidence of a comprehensive cross-talk mechanism between fluoride and obesity in HFD fed mice, which is mediated by gut microbiota and intestinal barrier. E. ramosum was identified as a crucial mediator of fluoride induced obesity, which could be explored as potential target for prevention and treatment of obesity with exciting translational value.

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Fluoride Depletes Acidogenic Taxa in Oral but Not Gut Microbial Communities in Mice

Cited by 23 publications

References 47 publications

Micronutrients impact the gut microbiota and blood glucose

Micronutrients impact the gut microbiota and blood glucose

Lactobacillus johnsonii BS15 improves intestinal environment against fluoride-induced memory impairment in mice—a study based on the gut–brain axis hypothesis

Fluoride Induced Leaky Gut and Bloom of Erysipelatoclostridium Ramosum Mediate the Exacerbation of Obesity in High-Fat-Diet Fed Mice

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