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      Dysbiosis and compositional alterations with aging in the gut microbiota of patients with heart failure

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          Abstract

          Emerging evidence has suggested a potential impact of gut microbiota on the pathophysiology of heart failure (HF). However, it is still unknown whether HF is associated with dysbiosis in gut microbiota. We investigated the composition of gut microbiota in patients with HF to elucidate whether gut microbial dysbiosis is associated with HF. We performed 16S ribosomal RNA gene sequencing of fecal samples obtained from 12 HF patients and 12 age-matched healthy control (HC) subjects, and analyzed the differences in gut microbiota. We further compared the composition of gut microbiota of 12 HF patients younger than 60 years of age with that of 10 HF patients 60 years of age or older. The composition of gut microbial communities of HF patients was distinct from that of HC subjects in both unweighted and weighted UniFrac analyses. Eubacterium rectale and Dorea longicatena were less abundant in the gut microbiota of HF patients than in that of HC subjects. Compared to younger HF patients, older HF patients had diminished proportions of Bacteroidetes and larger quantities of Proteobacteria. The genus Faecalibacterium was depleted, while Lactobacillus was enriched in the gut microbiota of older HF patients. These results suggest that patients with HF harbor significantly altered gut microbiota, which varies further according to age. New concept of heart-gut axis has a great potential for breakthroughs in the development of novel diagnostic and therapeutic approach for HF.

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          Most cited references 16

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          Intestinal Microbiota Composition Modulates Choline Bioavailability from Diet and Accumulation of the Proatherogenic Metabolite Trimethylamine-N-Oxide

          ABSTRACT Choline is a water-soluble nutrient essential for human life. Gut microbial metabolism of choline results in the production of trimethylamine (TMA), which upon absorption by the host is converted in the liver to trimethylamine-N-oxide (TMAO). Recent studies revealed that TMAO exacerbates atherosclerosis in mice and positively correlates with the severity of this disease in humans. However, which microbes contribute to TMA production in the human gut, the extent to which host factors (e.g., genotype) and diet affect TMA production and colonization of these microbes, and the effects TMA-producing microbes have on the bioavailability of dietary choline remain largely unknown. We screened a collection of 79 sequenced human intestinal isolates encompassing the major phyla found in the human gut and identified nine strains capable of producing TMA from choline in vitro. Gnotobiotic mouse studies showed that TMAO accumulates in the serum of animals colonized with TMA-producing species, but not in the serum of animals colonized with intestinal isolates that do not generate TMA from choline in vitro. Remarkably, low levels of colonization by TMA-producing bacteria significantly reduced choline levels available to the host. This effect was more pronounced as the abundance of TMA-producing bacteria increased. Our findings provide a framework for designing strategies aimed at changing the representation or activity of TMA-producing bacteria in the human gut and suggest that the TMA-producing status of the gut microbiota should be considered when making recommendations about choline intake requirements for humans.
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            Antimicrobial defense of the intestine.

            The mammalian gastrointestinal tract is home to a dense community of resident bacteria and is also exposed to microorganisms from the external environment. The epithelial surface of the intestine plays a critical role in host protection by producing a diverse repertoire of antimicrobial proteins that directly kill or hinder the growth of microorganisms. Here we discuss the general principles that govern the mechanisms of action of epithelial antimicrobial proteins, regulation of antimicrobial protein expression and activity, and in vivo functions of intestinal antimicrobial proteins. We also consider how altered antimicrobial protein expression and function can contribute to disease and how these endogenous antibiotics might be harnessed for the benefit of human health.
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              Abdominal contributions to cardiorenal dysfunction in congestive heart failure.

              Current pathophysiological models of congestive heart failure unsatisfactorily explain the detrimental link between congestion and cardiorenal function. Abdominal congestion (i.e., splanchnic venous and interstitial congestion) manifests in a substantial number of patients with advanced congestive heart failure, yet is poorly defined. Compromised capacitance function of the splanchnic vasculature and deficient abdominal lymph flow resulting in interstitial edema might both be implied in the occurrence of increased cardiac filling pressures and renal dysfunction. Indeed, increased intra-abdominal pressure, as an extreme marker of abdominal congestion, is correlated with renal dysfunction in advanced congestive heart failure. Intriguing findings provide preliminary evidence that alterations in the liver and spleen contribute to systemic congestion in heart failure. Finally, gut-derived hormones might influence sodium homeostasis, whereas entrance of bowel toxins into the circulatory system, as a result of impaired intestinal barrier function secondary to congestion, might further depress cardiac as well as renal function. Those toxins are mainly produced by micro-organisms in the gut lumen, with presumably important alterations in advanced heart failure, especially when renal function is depressed. Therefore, in this state-of-the-art review, we explore the crosstalk between the abdomen, heart, and kidneys in congestive heart failure. This might offer new diagnostic opportunities as well as treatment strategies to achieve decongestion in heart failure, especially when abdominal congestion is present. Among those currently under investigation are paracentesis, ultrafiltration, peritoneal dialysis, oral sodium binders, vasodilator therapy, renal sympathetic denervation and agents targeting the gut microbiota.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, CA USA )
                1932-6203
                22 March 2017
                2017
                : 12
                : 3
                Affiliations
                [1 ]Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
                [2 ]Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Japan
                [3 ]Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan
                [4 ]Department of Advanced Clinical Science and Therapeutics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
                [5 ]RIKEN Center for Integrative Medical Sciences, Yokohama, Japan
                [6 ]Graduate School of Environmental and Life Science, Okayama University, Okayama, Japan
                [7 ]Graduate School of Advanced Science and Engineering, Waseda University, Tokyo, Japan
                Nagoya University, JAPAN
                Author notes

                Competing Interests: The study was supported in part by Takeda Pharmaceutical Co., Ltd., Daiichi Sankyo Co., Ltd., Shionogi & Co., Ltd., Nippon Boehringer Ingelheim Co., Ltd., Bristol-Myers Squibb K.K., MSD K.K., Sanofi K.K., and Sumitomo Dainippon Pharma Co., Ltd. There are no patents, products in development, or marketed products to declare.

                • Conceptualization: HA IK.

                • Data curation: WS M. Hattori.

                • Formal analysis: SN ATN NT M. Harada HT HK YI ET JS.

                • Funding acquisition: HA.

                • Investigation: WS HM.

                • Methodology: KH HM M.Hattori.

                • Resources: TK ASK YS HY QL.

                • Writing – original draft: TK.

                • Writing – review & editing: HA IK.

                Article
                PONE-D-16-46082
                10.1371/journal.pone.0174099
                5362204
                28328981
                © 2017 Kamo et al

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                Page count
                Figures: 4, Tables: 0, Pages: 14
                Product
                Funding
                Funded by: funder-id http://dx.doi.org/10.13039/501100001691, Japan Society for the Promotion of Science;
                Award ID: KAKENHI 26670395
                Award Recipient :
                Funded by: Takeda Pharmaceutical Co., Ltd.
                Award Recipient :
                Funded by: Daiichi Sankyo Co., Ltd.
                Award Recipient :
                Funded by: funder-id http://dx.doi.org/10.13039/501100005612, Shionogi;
                Award Recipient :
                Funded by: Nippon Boehringer Ingelheim Co., Ltd.
                Award Recipient :
                Funded by: Bristol-Myers Squibb K.K.
                Award Recipient :
                Funded by: MSD K.K.
                Award Recipient :
                Funded by: Sanofi K.K.
                Award Recipient :
                Funded by: Sumitomo Dainippon Pharma Co., Ltd.
                Award Recipient :
                Funded by: funder-id http://dx.doi.org/10.13039/100009619, Japan Agency for Medical Research and Development;
                Award ID: M1501
                Award Recipient :
                Funded by: funder-id http://dx.doi.org/10.13039/100009619, Japan Agency for Medical Research and Development;
                Award ID: M1501
                Award Recipient :
                This work was supported in part by grants from Japan Society for the Promotion of Science (KAKENHI 26670395, https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-26670395/) to H.A., and Core Research for Evolutionary Medical Science and Technology (CREST) from Japan Agency for Medical Research and Development (AMED) (M1501, http://www.amed.go.jp/program/list/01/07/023_02.html) to K.H., H.M. H.A. has received research funding from Takeda Pharmaceutical Co., Ltd., Daiichi Sankyo Co., Ltd., Shionogi & Co., Ltd., Nippon Boehringer Ingelheim Co., Ltd., Bristol-Myers Squibb K.K., MSD K.K., Sanofi K.K., and Sumitomo Dainippon Pharma Co., Ltd. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. This does not alter our adherence to PLOS ONE policies on sharing data and materials.
                Categories
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                Medicine and Health Sciences
                Cardiology
                Heart Failure
                Biology and Life Sciences
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