Erratum: Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells

Furusawa, Yukihiro; Obata, Yuichi; Fukuda, Shinji; Endo, Takaho A.; Nakato, Gaku; Takahashi, Daisuke; Nakanishi, Yumiko; Uetake, Chikako; Kato, Keiko; Kato, Tamotsu; Takahashi, Mayuko; Fukuda, Noriko; Murakami, S.; Miyauchi, Eiji; Hino, Shingo; Atarashi, Koji; Onawa, Satoshi; Fujimura, Y; Lockett, Trevor; Clarke, Jane; Topping, David L.; Tomita, Masaru; Hori, Shohei; Ohara, Osamu; Morita, Tatsuya; Koseki, Haruhiko; Kikuchi, Jun; Honda, Kenya; Hase, Koji; Ohno, Hiroshi

doi:10.1038/nature13041

Cited by 24 publications

(19 citation statements)

References 1 publication

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“…Butyric acid is used as a major energy source by epithelial cells in the mucous membrane of the large intestine; it inhibits the growth of colorectal cancer cells and induces differentiation and apoptosis of them [32][33][34][35][36]. Butyric acid promotes the maturation of acquired immune system cells that play a central role in suppressing inflammation and allergic reactions [37][38]. It also inhibits the production of inflammatory cytokines [39].…”

Section: Discussionmentioning

confidence: 99%

Fecal microbiota transplantation as a new treatment for canine inflammatory bowel disease

Niina

Kibe

Suzuki

et al. 2021

Bioscience of Microbiota, Food and Health

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Section: Discussionmentioning

confidence: 99%

Fecal microbiota transplantation as a new treatment for canine inflammatory bowel disease

Niina

Kibe

Suzuki

et al. 2021

Bioscience of Microbiota, Food and Health

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“…Prevotellaceae is a well-known and often discussed genus in the phylum of Bacteroidetes. As a 'fermenting' group of bacteria, Prevotellaceae produce butyrate, which has been identified as a specific inducer of Treg cell differentiation [34]. The relative abundance of Prevotellaceae was also significantly higher in autoimmune disease, such as Graves' disease (GD), irritable bowel syndrome (IBS) and Crohn's disease [35][36].…”

Section: Discussionmentioning

confidence: 99%

SCFA producing bacteria shape the subtype of ADHD in children

Fan¹,

Li²,

Rui³

et al. 2019

Preprint

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There is little data on population-based identification of the gut microbiota with ADHD subtypes in children, yet whether the degree ADHD is characterized by short-chain fatty acids (SCFAs) remains unclear. We enrolled 59 ADHD children including 21 inattentive subtypes (ADHD-I), 20 combined subtypes (ADHD-C), 18 hyperactive-Impulsive subtypes (ADHD-H) and 23 healthy controls. The microbiota was characterized by 16S rRNA gene sequencing, and SCFA concentrations were determined by gas chromatographic analysis. Compared to the controls, we observed a decrease of 14 genera belonging to Ruminococcaceae, Lachnospiraceae, Verrucomicrobiaceae and Rikenellaceae family in ADHD-I, while Megamonas, Coprococcus_2 and Paraprevotella were significantly increased in ADHD-C. In addition, a lower abundance of Faecalibacterium, and a higher proportion of Marvinbryantia, Intestinimonas, Prevotella_9 and Eggerthella were detected in the ADHD-H. Analysis of fecal SCFAs showed that elevated levels of acetate and propionate were in ADHD subtypes. Furthermore, most of the bacterium associated with SCFAs overlapped with the differential bacterium in ADHD subtypes. Conclusion: Our data support the clinical distinction among different ADHD subtypes in children may also be reflected in alterations of specific gut microbiota, most of which are SCFA producing bacteria.

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“…In this context, it is important that we better understand which Tregs could be leveraged to prevent or halt the autoimmune response that underlies T1D. pTregs may constitute a subset amenable to therapeutic manipulation, owing to the fact that these cells can be induced within the mature T cell population by various agents, including microbial metabolites [37][38][39]. While inducing pTregs appears feasible, the extent to which these cells contribute to the control of pancreatic autoimmunity had not yet been established.…”

Section: Discussionmentioning

confidence: 99%

Peripherally-induced regulatory T cells contribute to the control of autoimmune diabetes

Schuster

Zhao

Kissler

2017

Preprint

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Type 1 diabetes (T1D) results from the autoimmune destruction of pancreatic beta cells and is partly caused by deficiencies in the Foxp3 + regulatory T cell (Treg) compartment. Conversely, therapies that increase Treg function can prevent autoimmune diabetes in animal models. The majority of Tregs develop in the thymus (tTregs), but a proportion of Foxp3 + Tregs is generated in the periphery (pTregs) from Foxp3 -CD4 + T cell precursors. Whether pTregs play a distinct role in T1D has not yet been explored. We report here that pTregs are a key modifier of disease in the nonobesed diabetic (NOD) mouse model for T1D. We generated NOD mice deficient for the Foxp3 enhancer CNS1 involved in pTreg induction. We show that CNS1 knockout decreased the frequency of pTregs and increased the risk of diabetes. Our results show that pTregs fulfill an important non-redundant function in the prevention of beta cell autoimmunity that causes T1D.

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Erratum: Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells

Abstract: In Fig. 1d of this Letter, the vertical label of the upper right panel should be ''Neuropilin-1 1 Foxp3 1 (%)'' instead of ''Neuropilin-1 2 / Foxp31 (%)''; this error has been corrected in the online versions of the paper.

Cited by 24 publications

References 1 publication

Fecal microbiota transplantation as a new treatment for canine inflammatory bowel disease

Fecal microbiota transplantation as a new treatment for canine inflammatory bowel disease

SCFA producing bacteria shape the subtype of ADHD in children

Peripherally-induced regulatory T cells contribute to the control of autoimmune diabetes

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