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      A Tryptophan-Deficient Diet Induces Gut Microbiota Dysbiosis and Increases Systemic Inflammation in Aged Mice

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          Abstract

          The gut microflora is a vital component of the gastrointestinal (GI) system that regulates local and systemic immunity, inflammatory response, the digestive system, and overall health. Older people commonly suffer from inadequate nutrition or poor diets, which could potentially alter the gut microbiota. The essential amino acid (AA) tryptophan (TRP) is a vital diet component that plays a critical role in physiological stress responses, neuropsychiatric health, oxidative systems, inflammatory responses, and GI health. The present study investigates the relationship between varied TRP diets, the gut microbiome, and inflammatory responses in an aged mouse model. We fed aged mice either a TRP-deficient (0.1%), TRP-recommended (0.2%), or high-TRP (1.25%) diet for eight weeks and observed changes in the gut bacterial environment and the inflammatory responses via cytokine analysis (IL-1a, IL-6, IL-17A, and IL-27). The mice on the TRP-deficient diets showed changes in their bacterial abundance of Coriobacteriia class, Acetatifactor genus, Lachnospiraceae family, Enterococcus faecalis species, Clostridium sp genus, and Oscillibacter genus. Further, these mice showed significant increases in IL-6, IL-17A, and IL-1a and decreased IL-27 levels. These data suggest a direct association between dietary TRP content, the gut microbiota microenvironment, and inflammatory responses in aged mice models.

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          Most cited references43

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          A metagenome-wide association study of gut microbiota in type 2 diabetes.

          Assessment and characterization of gut microbiota has become a major research area in human disease, including type 2 diabetes, the most prevalent endocrine disease worldwide. To carry out analysis on gut microbial content in patients with type 2 diabetes, we developed a protocol for a metagenome-wide association study (MGWAS) and undertook a two-stage MGWAS based on deep shotgun sequencing of the gut microbial DNA from 345 Chinese individuals. We identified and validated approximately 60,000 type-2-diabetes-associated markers and established the concept of a metagenomic linkage group, enabling taxonomic species-level analyses. MGWAS analysis showed that patients with type 2 diabetes were characterized by a moderate degree of gut microbial dysbiosis, a decrease in the abundance of some universal butyrate-producing bacteria and an increase in various opportunistic pathogens, as well as an enrichment of other microbial functions conferring sulphate reduction and oxidative stress resistance. An analysis of 23 additional individuals demonstrated that these gut microbial markers might be useful for classifying type 2 diabetes.
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            Linking long-term dietary patterns with gut microbial enterotypes.

            Diet strongly affects human health, partly by modulating gut microbiome composition. We used diet inventories and 16S rDNA sequencing to characterize fecal samples from 98 individuals. Fecal communities clustered into enterotypes distinguished primarily by levels of Bacteroides and Prevotella. Enterotypes were strongly associated with long-term diets, particularly protein and animal fat (Bacteroides) versus carbohydrates (Prevotella). A controlled-feeding study of 10 subjects showed that microbiome composition changed detectably within 24 hours of initiating a high-fat/low-fiber or low-fat/high-fiber diet, but that enterotype identity remained stable during the 10-day study. Thus, alternative enterotype states are associated with long-term diet.
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              Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis.

              The gastrointestinal (GI) tract contains much of the body's serotonin (5-hydroxytryptamine, 5-HT), but mechanisms controlling the metabolism of gut-derived 5-HT remain unclear. Here, we demonstrate that the microbiota plays a critical role in regulating host 5-HT. Indigenous spore-forming bacteria (Sp) from the mouse and human microbiota promote 5-HT biosynthesis from colonic enterochromaffin cells (ECs), which supply 5-HT to the mucosa, lumen, and circulating platelets. Importantly, microbiota-dependent effects on gut 5-HT significantly impact host physiology, modulating GI motility and platelet function. We identify select fecal metabolites that are increased by Sp and that elevate 5-HT in chromaffin cell cultures, suggesting direct metabolic signaling of gut microbes to ECs. Furthermore, elevating luminal concentrations of particular microbial metabolites increases colonic and blood 5-HT in germ-free mice. Altogether, these findings demonstrate that Sp are important modulators of host 5-HT and further highlight a key role for host-microbiota interactions in regulating fundamental 5-HT-related biological processes.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                08 May 2021
                May 2021
                : 22
                : 9
                : 5005
                Affiliations
                [1 ]Department of Medicine, Augusta University, Augusta, GA 30912, USA; IYUSUFU@ 123456augusta.edu (I.Y.); KDING@ 123456augusta.edu (K.D.); GPATTERSON1@ 123456augusta.edu (G.T.P.)
                [2 ]Department of Cell Biology and Anatomy, Augusta University, Augusta, GA 30912, USA; KATSMITH4@ 123456augusta.edu (K.S.); mhamrick@ 123456augusta.edu (M.W.H.)
                [3 ]Department of Pediatrics, College of Medicine, University of Arkansas for Medical Sciences (UAMS), Little Rock, AR 72202, USA; UWankhade@ 123456uams.edu
                [4 ]Arkansas Children Nutrition Center, Arkansas Children’s Research Institute, Little Rock, AR 72202, USA
                [5 ]Department of Infectious Diseases and Immunology, University of Florida, Gainesville, FL 32608, USA; sahayb@ 123456ufl.edu
                [6 ]Georgia Cancer Center, Augusta University, Augusta, GA 30902, USA; RPACHOLCZYK@ 123456augusta.edu
                [7 ]Department of Pathology, University of Notre Dame, Notre Dame, IN 46556, USA; sadusumi@ 123456nd.edu
                [8 ]Institute of Healthy Aging, Augusta University, Augusta, GA 30912, USA
                [9 ]Department of Pathology, Medical University of South Carolina, Charleston, SC 29403, USA; hillwi@ 123456musc.edu
                [10 ]Ralph H Johnson Veterans Affairs Medical Center, Charleston, SC 29403, USA
                Author notes
                [* ]Correspondence: cisales@ 123456augusta.edu (C.M.I.); sfulzele@ 123456augusta.edu (S.F.)
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0003-4810-221X
                https://orcid.org/0000-0002-9629-4829
                https://orcid.org/0000-0002-4480-3484
                Article
                ijms-22-05005
                10.3390/ijms22095005
                8125914
                34066870
                5d64b62e-5b51-450c-92b0-ffa4f9ecc707
                © 2021 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( https://creativecommons.org/licenses/by/4.0/).

                History
                : 07 April 2021
                : 03 May 2021
                Categories
                Article

                Molecular biology
                tryptophan,systemic inflammation,dysbiosis,gut,microbiota
                Molecular biology
                tryptophan, systemic inflammation, dysbiosis, gut, microbiota

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