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  1. Article ; Online: Diet, commensal microbiota-derived extracellular vesicles, and host immunity.

    Taitz, Jemma J / Tan, Jian K / Potier-Villette, Camille / Ni, Duan / King, Nicholas Jc / Nanan, Ralph / Macia, Laurence

    European journal of immunology

    2023  Volume 53, Issue 7, Page(s) e2250163

    Abstract: The gut microbiota has co-evolved with its host, and commensal bacteria can influence both the host's immune development and function. Recently, a role has emerged for bacterial extracellular vesicles (BEVs) as potent immune modulators. BEVs are ... ...

    Abstract The gut microbiota has co-evolved with its host, and commensal bacteria can influence both the host's immune development and function. Recently, a role has emerged for bacterial extracellular vesicles (BEVs) as potent immune modulators. BEVs are nanosized membrane vesicles produced by all bacteria, possessing the membrane characteristics of the originating bacterium and carrying an internal cargo that may include nucleic acid, proteins, lipids, and metabolites. Thus, BEVs possess multiple avenues for regulating immune processes, and have been implicated in allergic, autoimmune, and metabolic diseases. BEVs are biodistributed locally in the gut, and also systemically, and thus have the potential to affect both the local and systemic immune responses. The production of gut microbiota-derived BEVs is regulated by host factors such as diet and antibiotic usage. Specifically, all aspects of nutrition, including macronutrients (protein, carbohydrates, and fat), micronutrients (vitamins and minerals), and food additives (the antimicrobial sodium benzoate), can regulate BEV production. This review summarizes current knowledge of the powerful links between nutrition, antibiotics, gut microbiota-derived BEV, and their effects on immunity and disease development. It highlights the potential of targeting or utilizing gut microbiota-derived BEV as a therapeutic intervention.
    MeSH term(s) Microbiota ; Diet ; Gastrointestinal Microbiome/physiology ; Bacteria ; Anti-Bacterial Agents ; Extracellular Vesicles/metabolism
    Chemical Substances Anti-Bacterial Agents
    Language English
    Publishing date 2023-05-17
    Publishing country Germany
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 120108-6
    ISSN 1521-4141 ; 0014-2980
    ISSN (online) 1521-4141
    ISSN 0014-2980
    DOI 10.1002/eji.202250163
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Myeloperoxidase Gene Deletion Causes Drastic Microbiome Shifts in Mice and Does Not Mitigate Dextran Sodium Sulphate-Induced Colitis.

    San Gabriel, Patrick T / O'Neil, Thomas R / Au, Alice / Tan, Jian K / Pinget, Gabriela V / Liu, Yuyang / Fong, Genevieve / Ku, Jacqueline / Glaros, Elias / Macia, Laurence / Witting, Paul K / Thomas, Shane R / Chami, Belal

    International journal of molecular sciences

    2024  Volume 25, Issue 8

    Abstract: Neutrophil-myeloperoxidase (MPO) is a heme-containing peroxidase which produces excess amounts of hypochlorous acid during inflammation. While pharmacological MPO inhibition mitigates all indices of experimental colitis, no studies have corroborated the ... ...

    Abstract Neutrophil-myeloperoxidase (MPO) is a heme-containing peroxidase which produces excess amounts of hypochlorous acid during inflammation. While pharmacological MPO inhibition mitigates all indices of experimental colitis, no studies have corroborated the role of MPO using knockout (KO) models. Therefore, we investigated MPO deficient mice in a murine model of colitis. Wild type (Wt) and MPO-deficient mice were treated with dextran sodium sulphate (DSS) in a chronic model of experimental colitis with three acute cycles of DSS-induced colitis over 63 days, emulating IBD relapse and remission cycles. Mice were immunologically profiled at the gut muscoa and the faecal microbiome was assessed via 16S rRNA amplicon sequencing. Contrary to previous pharmacological antagonist studies targeting MPO, MPO-deficient mice showed no protection from experimental colitis during cyclical DSS-challenge. We are the first to report drastic faecal microbiota shifts in MPO-deficient mice, showing a significantly different microbiome profile on Day 1 of treatment, with a similar shift and distinction on Day 29 (half-way point), via qualitative and quantitative descriptions of phylogenetic distances. Herein, we provide the first evidence of substantial microbiome shifts in MPO-deficiency, which may influence disease progression. Our findings have significant implications for the utility of MPO-KO mice in investigating disease models.
    MeSH term(s) Animals ; Dextran Sulfate ; Peroxidase/metabolism ; Peroxidase/genetics ; Mice ; Colitis/microbiology ; Colitis/chemically induced ; Colitis/genetics ; Mice, Knockout ; Gastrointestinal Microbiome ; Disease Models, Animal ; Feces/microbiology ; Gene Deletion ; RNA, Ribosomal, 16S/genetics ; Mice, Inbred C57BL
    Chemical Substances Dextran Sulfate (9042-14-2) ; Peroxidase (EC 1.11.1.7) ; RNA, Ribosomal, 16S
    Language English
    Publishing date 2024-04-11
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms25084258
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The water chemistry and microbiome of household wells in Medawachchiya, Sri Lanka, an area with high prevalence of chronic kidney disease of unknown origin (CKDu).

    McDonough, Liza K / Meredith, Karina T / Nikagolla, Chandima / Middleton, Ryan J / Tan, Jian K / Ranasinghe, Asanga V / Sierro, Frederic / Banati, Richard B

    Scientific reports

    2020  Volume 10, Issue 1, Page(s) 18295

    Abstract: Chronic kidney disease (CKD) of unknown etiology (CKDu) mostly affects agricultural communities in Central America, South Asia, Africa, but likely also in North America and Australia. One such area with increased CKDu prevalence is the Medawachchiya ... ...

    Abstract Chronic kidney disease (CKD) of unknown etiology (CKDu) mostly affects agricultural communities in Central America, South Asia, Africa, but likely also in North America and Australia. One such area with increased CKDu prevalence is the Medawachchiya District Secretariat Division of the Anuradhapura District in the North Central Province of Sri Lanka. Recent research has focused on the presence of various microbial pathogens in drinking water as potential causal or contributing factors to CKDu, yet no study to date has performed a more comprehensive microbial and water chemistry assessment of household wells used for domestic water supply in areas of high CKDu prevalence. In this study, we describe the chemical composition and total microbial content in 30 domestic household wells in the Medawachchiya District Secretariat Division. While the chemical composition in the tested wells mostly lies within standard drinking water limits, except for high levels of fluoride (F), magnesium (Mg), sodium (Na), chloride (Cl) and calcium (Ca) in some samples, we find a frequent presence of cyanotoxin-producing Microcystis, confirming earlier studies in Sri Lanka. Since the total microbial content of drinking water also directly influences the composition of the human gut microbiome, it can be considered an important determinant of health. Several bacterial phyla were previously reported in the gut microbiome of patients with CKD. Using these bacteria phyla to define operational taxonomic units, we found that these bacteria also occur in the microbiome of the sampled well water. Based on available environmental data, our study demonstrates associations between the abundances of these bacteria with geographical distribution, well water temperature and likely fertilizer use in the local surface water catchment area of the individual household wells. Our results reinforce the recommendation that household wells with stagnant or infrequently used water should be purged prior to use for drinking water, bathing and irrigation. The latter is suggested because of the reported potential accumulation of bacterial toxins by agricultural crops. The observation that bacteria previously found in chronic kidney disease patients are also present in household wells requires a more detailed systematic study of both the human gut and drinking water microbiomes in CKDu patients, in relation to disease prevalence and progression.
    MeSH term(s) Bacteria/classification ; Bacteria/isolation & purification ; Disease Progression ; Drinking Water/analysis ; Drinking Water/chemistry ; Drinking Water/microbiology ; Gastrointestinal Microbiome ; Humans ; Phylogeny ; Prevalence ; Renal Insufficiency, Chronic/epidemiology ; Renal Insufficiency, Chronic/etiology ; Sri Lanka/epidemiology ; Water Microbiology ; Water Pollutants, Chemical/analysis ; Water Wells
    Chemical Substances Drinking Water ; Water Pollutants, Chemical
    Language English
    Publishing date 2020-10-26
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-020-75336-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Metabolite-Sensing G Protein-Coupled Receptors-Facilitators of Diet-Related Immune Regulation.

    Tan, Jian K / McKenzie, Craig / Mariño, Eliana / Macia, Laurence / Mackay, Charles R

    Annual review of immunology

    2017  Volume 35, Page(s) 371–402

    Abstract: Nutrition and the gut microbiome regulate many systems, including the immune, metabolic, and nervous systems. We propose that the host responds to deficiency (or sufficiency) of dietary and bacterial metabolites in a dynamic way, to optimize responses ... ...

    Abstract Nutrition and the gut microbiome regulate many systems, including the immune, metabolic, and nervous systems. We propose that the host responds to deficiency (or sufficiency) of dietary and bacterial metabolites in a dynamic way, to optimize responses and survival. A family of G protein-coupled receptors (GPCRs) termed the metabolite-sensing GPCRs bind to various metabolites and transmit signals that are important for proper immune and metabolic functions. Members of this family include GPR43, GPR41, GPR109A, GPR120, GPR40, GPR84, GPR35, and GPR91. In addition, bile acid receptors such as GPR131 (TGR5) and proton-sensing receptors such as GPR65 show similar features. A consistent feature of this family of GPCRs is that they provide anti-inflammatory signals; many also regulate metabolism and gut homeostasis. These receptors represent one of the main mechanisms whereby the gut microbiome affects vertebrate physiology, and they also provide a link between the immune and metabolic systems. Insufficient signaling through one or more of these metabolite-sensing GPCRs likely contributes to human diseases such as asthma, food allergies, type 1 and type 2 diabetes, hepatic steatosis, cardiovascular disease, and inflammatory bowel diseases.
    MeSH term(s) Animals ; Cardiovascular Diseases/immunology ; Diabetes Mellitus, Type 1/immunology ; Diet ; Gastrointestinal Microbiome/immunology ; Homeostasis ; Humans ; Hypersensitivity/immunology ; Immunity ; Inflammatory Bowel Diseases/immunology ; Intestines/metabolism ; Receptors, G-Protein-Coupled/immunology ; Receptors, G-Protein-Coupled/metabolism
    Chemical Substances Receptors, G-Protein-Coupled
    Language English
    Publishing date 2017-04-26
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 604953-9
    ISSN 1545-3278 ; 0732-0582
    ISSN (online) 1545-3278
    ISSN 0732-0582
    DOI 10.1146/annurev-immunol-051116-052235
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: High-Fiber Diet and Acetate Supplementation Change the Gut Microbiota and Prevent the Development of Hypertension and Heart Failure in Hypertensive Mice.

    Marques, Francine Z / Nelson, Erin / Chu, Po-Yin / Horlock, Duncan / Fiedler, April / Ziemann, Mark / Tan, Jian K / Kuruppu, Sanjaya / Rajapakse, Niwanthi W / El-Osta, Assam / Mackay, Charles R / Kaye, David M

    Circulation

    2017  Volume 135, Issue 10, Page(s) 964–977

    Abstract: Background: Dietary intake of fruit and vegetables is associated with lower incidence of hypertension, but the mechanisms involved have not been elucidated. Here, we evaluated the effect of a high-fiber diet and supplementation with the short-chain ... ...

    Abstract Background: Dietary intake of fruit and vegetables is associated with lower incidence of hypertension, but the mechanisms involved have not been elucidated. Here, we evaluated the effect of a high-fiber diet and supplementation with the short-chain fatty acid acetate on the gut microbiota and the prevention of cardiovascular disease.
    Methods: Gut microbiome, cardiorenal structure/function, and blood pressure were examined in sham and mineralocorticoid excess-treated mice with a control diet, high-fiber diet, or acetate supplementation. We also determined the renal and cardiac transcriptome of mice treated with the different diets.
    Results: We found that high consumption of fiber modified the gut microbiota populations and increased the abundance of acetate-producing bacteria independently of mineralocorticoid excess. Both fiber and acetate decreased gut dysbiosis, measured by the ratio of Firmicutes to Bacteroidetes, and increased the prevalence of
    Conclusions: A diet high in fiber led to changes in the gut microbiota that played a protective role in the development of cardiovascular disease. The favorable effects of fiber may be explained by the generation and distribution of one of the main metabolites of the gut microbiota, the short-chain fatty acid acetate. Acetate effected several molecular changes associated with improved cardiovascular health and function.
    MeSH term(s) Animals ; Bacteria/genetics ; Bacteria/isolation & purification ; Blood Pressure/drug effects ; Desoxycorticosterone Acetate/pharmacology ; Desoxycorticosterone Acetate/therapeutic use ; Dietary Fiber/pharmacology ; Dietary Fiber/therapeutic use ; Dietary Supplements ; Disease Models, Animal ; Fibrosis ; Gastrointestinal Microbiome/drug effects ; Gastrointestinal Tract/microbiology ; Hypertension/pathology ; Hypertension/prevention & control ; Hypertension/veterinary ; Kidney/metabolism ; Kidney/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Myocardium/metabolism ; Myocardium/pathology ; Organ Size/drug effects ; Principal Component Analysis ; RNA, Ribosomal, 16S/chemistry ; RNA, Ribosomal, 16S/genetics ; RNA, Ribosomal, 16S/metabolism ; Transcriptome/drug effects
    Chemical Substances Dietary Fiber ; RNA, Ribosomal, 16S ; Desoxycorticosterone Acetate (6E0A168OB8)
    Language English
    Publishing date 2017-03-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.116.024545
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Avenues to autoimmune arthritis triggered by diverse remote inflammatory challenges.

    Chevalier, Nina / Tan, Jian K / Mason, Linda J / Robert, Remy / McKenzie, Craig I / Lim, Florence / Wong, Connie H / Macia, Laurence / Thorburn, Alison N / Russ, Brendan E / Masters, Seth L / Mackay, Charles R

    Journal of autoimmunity

    2016  Volume 73, Page(s) 120–129

    Abstract: Environmental factors contribute to development of autoimmune diseases. For instance, human autoimmune arthritis can associate with intestinal inflammation, cigarette smoking, periodontal disease, and various infections. The cellular and, molecular ... ...

    Abstract Environmental factors contribute to development of autoimmune diseases. For instance, human autoimmune arthritis can associate with intestinal inflammation, cigarette smoking, periodontal disease, and various infections. The cellular and, molecular pathways whereby such remote challenges might precipitate arthritis or flares remain unclear. Here, we used a transfer model of self-reactive arthritis-inducing CD4(+) cells from KRNtg mice that, upon transfer, induce a very mild form of autoinflammatory arthritis in recipient animals. This model enabled us to identify external factors that greatly aggravated disease. We show that several distinct challenges precipitated full-blown arthritis, including intestinal inflammation through DSS-induced colitis, and bronchial stress through Influenza infection. Both triggers induced strong IL-17 expression primarily in self-reactive CD4(+) cells in lymph nodes draining the site of inflammation. Moreover, treatment of mice with IL-1β greatly exacerbated arthritis, while transfer of KRNtg CD4(+) cells lacking IL-1R significantly reduced disease and IL-17 expression. Thus, IL-1β enhances the autoaggressive potential of self-reactive CD4(+) cells, through increased Th17 differentiation, and this influences inflammatory events in the joints. We propose that diverse challenges that cause remote inflammation (lung infection or colitis, etc.) result in IL-1β-driven Th17 differentiation, and this precipitates arthritis in genetically susceptible individuals. Thus the etiology of autoimmune inflammatory arthritis likely relates to diverse triggers that converge to a common pathway involving IL-1β production and Th17 cell distribution.
    MeSH term(s) Adoptive Transfer ; Animals ; Arthritis, Experimental/immunology ; Arthritis, Rheumatoid/genetics ; Arthritis, Rheumatoid/immunology ; CD4-Positive T-Lymphocytes/immunology ; Cell Differentiation/immunology ; Colitis/chemically induced ; Colitis/immunology ; Dextran Sulfate/toxicity ; Genetic Predisposition to Disease ; Influenza A virus/immunology ; Interleukin-17/metabolism ; Interleukin-1beta/metabolism ; Joints/immunology ; Klebsiella pneumoniae/immunology ; Lung Diseases/immunology ; Lung Diseases/virology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, Transgenic ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/virology ; Pneumonia, Bacterial/immunology ; Pneumonia, Bacterial/microbiology ; Receptors, Interleukin-1/genetics ; Receptors, Interleukin-1/metabolism ; Spondylarthritis/immunology ; Th17 Cells/immunology ; Th17 Cells/metabolism
    Chemical Substances IL1B protein, mouse ; Interleukin-17 ; Interleukin-1beta ; Receptors, Interleukin-1 ; Dextran Sulfate (9042-14-2)
    Language English
    Publishing date 2016
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639452-8
    ISSN 1095-9157 ; 0896-8411
    ISSN (online) 1095-9157
    ISSN 0896-8411
    DOI 10.1016/j.jaut.2016.06.018
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  7. Article ; Online: The Role of Follicular Helper T Cell Molecules and Environmental Influences in Autoantibody Production and Progression to Inflammatory Arthritis in Mice.

    Chevalier, Nina / Macia, Laurence / Tan, Jian K / Mason, Linda J / Robert, Remy / Thorburn, Alison N / Wong, Connie H Y / Tsai, Louis M / Bourne, Katherine / Brink, Robert / Yu, Di / Mackay, Charles R

    Arthritis & rheumatology (Hoboken, N.J.)

    2015  Volume 68, Issue 4, Page(s) 1026–1038

    Abstract: Objective: Antibody-mediated autoimmunity involves cognate interactions between self-reactive T cells and B cells during germinal center (GC) reactions. The aim of this study was to determine the role of essential follicular helper T (Tfh) cell ... ...

    Abstract Objective: Antibody-mediated autoimmunity involves cognate interactions between self-reactive T cells and B cells during germinal center (GC) reactions. The aim of this study was to determine the role of essential follicular helper T (Tfh) cell molecules (CXCR5, signaling lymphocytic activation molecule-associated protein) on autoreactive CD4+ cells and the role of certain environmental influences that may determine GC-driven autoantibody production and arthritis development.
    Methods: We transferred self-reactive CD4+ cells from KRN-Tg mice into recipient mice, which induced autoantibodies and autoinflammatory arthritis. This model allowed manipulation of environmental effects, such as inflammation, and use of transferred cells that were genetically deficient in important Tfh cell-associated molecules.
    Results: A deficiency of signaling lymphocytic activation molecule-associated protein (SAP) in CD4+ cells from KRN-Tg mice completely protected against arthritis, indicating that stable T cell-B cell interactions are required for GC formation, autoantibody production, and arthritis induction. In contrast, a CXCR5 deficiency in CD4+ cells from KRN-Tg mice still induced disease when these cells were transferred into wild-type mice, suggesting that T cell help for B cells could rely on other migration mechanisms. However, various manipulations influenced this system, including elimination of bystander effects through use of CD28(-/-) recipient mice (reduced disease) or use of inflammation-inducing Freund's complete adjuvant (progression to arthritis). We also examined the capacity of preexisting GCs with a nonautoimmune specificity to co-opt autoimmune T cells and observed no evidence for any influence.
    Conclusion: In addition to the quality and quantity of cognate CD4+ cell help, external factors such as inflammation and noncognate CD4+ cell bystander activation trigger autoimmunity by shaping events within autoimmune GC responses. SAP is an essential molecule for autoimmune antibody production, whereas the importance of CXCR5 varies depending on the circumstances.
    MeSH term(s) Animals ; Arthritis, Psoriatic/immunology ; Arthritis, Rheumatoid/genetics ; Arthritis, Rheumatoid/immunology ; Autoantibodies/biosynthesis ; Autoantibodies/immunology ; Autoimmune Diseases/immunology ; Disease Models, Animal ; Disease Progression ; Environment ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Germinal Center/cytology ; Glucose-6-Phosphate Isomerase/immunology ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/immunology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Real-Time Polymerase Chain Reaction ; Receptors, CXCR5/genetics ; Receptors, CXCR5/immunology ; Reverse Transcriptase Polymerase Chain Reaction ; Signaling Lymphocytic Activation Molecule Associated Protein ; T-Lymphocytes, Helper-Inducer/immunology
    Chemical Substances Autoantibodies ; CXCR5 protein, mouse ; Intracellular Signaling Peptides and Proteins ; Receptors, CXCR5 ; Sh2d1a protein, mouse ; Signaling Lymphocytic Activation Molecule Associated Protein ; Glucose-6-Phosphate Isomerase (EC 5.3.1.9)
    Language English
    Publishing date 2015-10-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.39481
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  8. Article ; Online: Evidence that asthma is a developmental origin disease influenced by maternal diet and bacterial metabolites.

    Thorburn, Alison N / McKenzie, Craig I / Shen, Sj / Stanley, Dragana / Macia, Laurence / Mason, Linda J / Roberts, Laura K / Wong, Connie H Y / Shim, Raymond / Robert, Remy / Chevalier, Nina / Tan, Jian K / Mariño, Eliana / Moore, Rob J / Wong, Lee / McConville, Malcolm J / Tull, Dedreia L / Wood, Lisa G / Murphy, Vanessa E /
    Mattes, Joerg / Gibson, Peter G / Mackay, Charles R

    Nature communications

    2015  Volume 6, Page(s) 7320

    Abstract: Asthma is prevalent in Western countries, and recent explanations have evoked the actions of the gut microbiota. Here we show that feeding mice a high-fibre diet yields a distinctive gut microbiota, which increases the levels of the short-chain fatty ... ...

    Abstract Asthma is prevalent in Western countries, and recent explanations have evoked the actions of the gut microbiota. Here we show that feeding mice a high-fibre diet yields a distinctive gut microbiota, which increases the levels of the short-chain fatty acid, acetate. High-fibre or acetate-feeding led to marked suppression of allergic airways disease (AAD, a model for human asthma), by enhancing T-regulatory cell numbers and function. Acetate increases acetylation at the Foxp3 promoter, likely through HDAC9 inhibition. Epigenetic effects of fibre/acetate in adult mice led us to examine the influence of maternal intake of fibre/acetate. High-fibre/acetate feeding of pregnant mice imparts on their adult offspring an inability to develop robust AAD. High fibre/acetate suppresses expression of certain genes in the mouse fetal lung linked to both human asthma and mouse AAD. Thus, diet acting on the gut microbiota profoundly influences airway responses, and may represent an approach to prevent asthma, including during pregnancy.
    MeSH term(s) Acetates/metabolism ; Acetates/pharmacology ; Acetylation/drug effects ; Animals ; Asthma/immunology ; Asthma/metabolism ; Diet ; Dietary Fiber/metabolism ; Disease Models, Animal ; Epigenesis, Genetic/drug effects ; Fatty Acids, Volatile/metabolism ; Fatty Acids, Volatile/pharmacology ; Female ; Forkhead Transcription Factors/drug effects ; Forkhead Transcription Factors/genetics ; Gastrointestinal Microbiome ; Histone Deacetylases/drug effects ; Histone Deacetylases/metabolism ; Mice ; Pregnancy ; Prenatal Exposure Delayed Effects/immunology ; Prenatal Exposure Delayed Effects/metabolism ; Promoter Regions, Genetic ; Repressor Proteins/drug effects ; Repressor Proteins/metabolism ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/immunology
    Chemical Substances Acetates ; Dietary Fiber ; Fatty Acids, Volatile ; Forkhead Transcription Factors ; Foxp3 protein, mouse ; Repressor Proteins ; Hdac9 protein, mouse (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98)
    Language English
    Publishing date 2015-06-23
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2041-1723
    ISSN (online) 2041-1723
    DOI 10.1038/ncomms8320
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