Bile acid metabolites control TH17 and Treg cell differentiation

Hang, Saiyu; Paik, Donggi; Yao, Lina; Kim, Eunha; Trinath, Jamma; Lu, Jiayi; Ha, Soyoung; Nelson, Brandon N.; Kelly, Samantha; Wu, Lin; Zheng, Ye; Longman, Randy S.; Rastinejad, Fraydoon; Devlin, A. Sloan; Krout, Michael R.; Fischbach, Michael A.; Littman, Dan R.; Huh, Jun R.

doi:10.1038/s41586-019-1785-z

Cited by 871 publications

(722 citation statements)

References 58 publications

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“…The effect of isoDCA on dendritic cells in this study is in contrast to recent work of T‐cell‐modulating bile acids, which potentiate Treg generation in a cell‐intrinsic manner 5,6 . This suggests that bile acids have diverse effects on the adaptive immune system and affect multiple cell types, opening the door for further research on how microbial metabolites can influence immune responses.…”

Section: Figurecontrasting

confidence: 76%

“…The molecular mechanism by which the microbiome interacts with peripherally induced Treg (pTreg) is likely complex and multifactorial; however, part of the effect is mediated via the release of microbial fermentation products, such as butyrate and other short‐chain fatty acids 1–3 . In a string of recent studies, a role for host bile acids has also been shown to induce pTreg generation, with this function dependent on commensal colonization 4–6 . In the recent issue of Nature , Rudensky and colleagues dissect the molecular fermentation pathway where the gut microbiome converts an endogenous bile acid into an immunologically active bile acid with the capacity to induce pTreg in the gut 4 …”

Section: Figurementioning

confidence: 99%

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Bile acids mediate signaling between microbiome and the immune system

Liston

Whyte

2020

Immunol Cell Biol

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Section: Figurecontrasting

confidence: 76%

Section: Figurementioning

confidence: 99%

Bile acids mediate signaling between microbiome and the immune system

Liston

Whyte

2020

Immunol Cell Biol

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“…One of these diseases is ulcerative colitis, an inflammatory bowel disease. Ketogenic diets may dampen inflammation within the gastrointestinal tract by inhibiting the activity of the NLRP3 inflammasome (8), promoting intestinal stem cell regeneration and gut healing (9), and stimulating the release of bile acids that facilitate intestinal immune system homeostasis (10,11).…”

Section: Introductionmentioning

confidence: 99%

A Standard Lipid Panel Is Insufficient for the Care of a Patient on a High-Fat, Low-Carbohydrate Ketogenic Diet

Norwitz

Loh

2020

Front. Med.

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High-fat, low-carbohydrate ketogenic diets have recently become popular for weight loss and the treatment of numerous chronic diseases; however, the general medical community still expresses concern regarding the impact of high-fat diets on serum lipids and cardiovascular risk. Herein, we report on a young man who adopted a ketogenic diet to treat his inflammatory bowel disease. Incidentally, changes in his serum lipids that would be considered adverse by current standards were noted. A more critical analysis of his lipid profile suggests that the changes he experienced may not be dangerous and may, at least with regard to several parameters, represent improvements. This case study demonstrates how the manner in which lipid panels are often reported and reviewed can lead to misleading conclusions and highlights that, at least in the care of those on a ketogenic diet, more nuanced analyses of lipid subfractionations should be conducted in order for physicians to provide optimal care and clinical recommendations.

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“…It is welldocumented that bile acid plays a potent regulation role on intestinal immunity cells [48]. A recently published paper in Nature demonstrated that bile acid metabolites can control Th17 and Treg cell differentiation [49]. In the present study, we found negative associations between hyodeoxycholic acid, isolithocholic acid, and TXB2, which were significantly decreased in the SA group, with serum cytokines, IL-17, TNF-α, and IFN-γ, and positive associations for chenodeoxycholic acid sulfate, L-Carnitine, acetylcholine, and cholic acid metabolites.…”

Section: Discussionmentioning

confidence: 99%

Gut Dysbacteriosis Is Associated with an Imbalanced Cytokines Network in Women with Unexplained Miscarriage

Liu

Chen

et al. 2020

Preprint

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Background: A dysregulation of cytokine networks has been suggested to be involved in the pathogenesis of unexplained pregnancy loss. Gut microbiota affects host immune response and induces an imbalance in cytokine levels. However, how gut microbial dysbiosis affects the disturbance of cellular immune function in spontaneous abortion (SA) patients remains inconclusive.Results: Serum proinflammatory cytokine levels were significantly increased in SA patients. Microbial diversity in patients with SA was reduced compared with that in the controls, as were the relative abundances of Prevotella_1, Prevotellaceae_UCG_003, and Selenomonas_1 were significantly reduced in the cases. Fecal metabolomics profiles were altered in SA patients, and the correlation analyses indicated that some microbe-associated metabolites, which were significantly enriched in bile secretion and histidine metabolism pathways, were positively associated with changes in levels of IL-17A, IL-17F, TNF-α, and IFN-γ in the SA group. Moreover, the microbial-associated metabolites, imidazolepropionic acid and 1, 4-Methylimidazoleacetic acid, are associated with recurrent pregnancy loss.Conclusions: Our study highlights the network among gut microbiome, fecal metabolites and Th1/Th17-mediated immune response in miscarriage patients and identifies potential novel biomarkers and an intervention target for recurrent miscarriage.

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Bile acid metabolites control TH17 and Treg cell differentiation

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Cited by 871 publications

References 58 publications

Bile acids mediate signaling between microbiome and the immune system

Bile acids mediate signaling between microbiome and the immune system

A Standard Lipid Panel Is Insufficient for the Care of a Patient on a High-Fat, Low-Carbohydrate Ketogenic Diet

Gut Dysbacteriosis Is Associated with an Imbalanced Cytokines Network in Women with Unexplained Miscarriage

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