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      (Dis)Trust your gut: the gut microbiome in age-related inflammation, health, and disease

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      Publication date (Electronic):
      Journal: Microbiome
      Publisher: BioMed Central

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          Abstract

          Chronic inflammation represents one of the most consistent biologic features of aging. However, the precise etiology of persistent low-grade increases in inflammation remains unclear. Recent evidence suggests that the gut microbiome may play a key role in age-related inflammation. Indeed, several studies have indicated that older adults display an altered composition of the gut microbiota, and early evidence indicates that this dysbiosis is associated with the presence of several key circulating inflammatory analytes. The present review summarizes knowledge on age-related inflammation and discusses how potential relationships with gut dysbiosis may lead to novel treatment strategies in the future.

          “The pattern of disease is an expression of the response of man to his total environment (physical, biological, and social); this response is, therefore, determined by anything that affects man himself or his environment.” – Rene Dubos, 1961

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          Role of the microbiota in immunity and inflammation.

          Yasmine Belkaid, Timothy Hand (2014)
          The microbiota plays a fundamental role on the induction, training, and function of the host immune system. In return, the immune system has largely evolved as a means to maintain the symbiotic relationship of the host with these highly diverse and evolving microbes. When operating optimally, this immune system-microbiota alliance allows the induction of protective responses to pathogens and the maintenance of regulatory pathways involved in the maintenance of tolerance to innocuous antigens. However, in high-income countries, overuse of antibiotics, changes in diet, and elimination of constitutive partners, such as nematodes, may have selected for a microbiota that lack the resilience and diversity required to establish balanced immune responses. This phenomenon is proposed to account for some of the dramatic rise in autoimmune and inflammatory disorders in parts of the world where our symbiotic relationship with the microbiota has been the most affected. Copyright © 2014 Elsevier Inc. All rights reserved.
          Article 0 comments Cited 1192 times – based on 0 reviews     Review now
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            Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis.

            Seth Rakoff-Nahoum, Justin Paglino, Fatima Eslami-Varzaneh … (2004)
            Toll-like receptors (TLRs) play a crucial role in host defense against microbial infection. The microbial ligands recognized by TLRs are not unique to pathogens, however, and are produced by both pathogenic and commensal microorganisms. It is thought that an inflammatory response to commensal bacteria is avoided due to sequestration of microflora by surface epithelia. Here, we show that commensal bacteria are recognized by TLRs under normal steady-state conditions, and this interaction plays a crucial role in the maintenance of intestinal epithelial homeostasis. Furthermore, we find that activation of TLRs by commensal microflora is critical for the protection against gut injury and associated mortality. These findings reveal a novel function of TLRs-control of intestinal epithelial homeostasis and protection from injury-and provide a new perspective on the evolution of host-microbial interactions.
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              Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson's Disease.

              Timothy Sampson, Justine W. Debelius, Taren Thron … (2016)
              The intestinal microbiota influence neurodevelopment, modulate behavior, and contribute to neurological disorders. However, a functional link between gut bacteria and neurodegenerative diseases remains unexplored. Synucleinopathies are characterized by aggregation of the protein α-synuclein (αSyn), often resulting in motor dysfunction as exemplified by Parkinson's disease (PD). Using mice that overexpress αSyn, we report herein that gut microbiota are required for motor deficits, microglia activation, and αSyn pathology. Antibiotic treatment ameliorates, while microbial re-colonization promotes, pathophysiology in adult animals, suggesting that postnatal signaling between the gut and the brain modulates disease. Indeed, oral administration of specific microbial metabolites to germ-free mice promotes neuroinflammation and motor symptoms. Remarkably, colonization of αSyn-overexpressing mice with microbiota from PD-affected patients enhances physical impairments compared to microbiota transplants from healthy human donors. These findings reveal that gut bacteria regulate movement disorders in mice and suggest that alterations in the human microbiome represent a risk factor for PD.
              Article 0 comments Cited 901 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Thomas W. Buford: twbuford@uab.edu
                Journal
                Journal ID (nlm-ta): Microbiome
                Journal ID (iso-abbrev): Microbiome
                Title: Microbiome
                Publisher: BioMed Central (London )
                ISSN (Electronic): 2049-2618
                Publication date (Electronic): 14 July 2017
                Publication date PMC-release: 14 July 2017
                Publication date Collection: 2017
                Volume: 5
                Electronic Location Identifier: 80
                Affiliations
                ISNI 0000000106344187, GRID grid.265892.2, Department of Medicine, , University of Alabama at Birmingham, ; 933 19th Street South, Birmingham, AL 35294 USA
                Article
                Publisher ID: 296
                DOI: 10.1186/s40168-017-0296-0
                PMC ID: 5512975
                PubMed ID: 28709450
                SO-VID: f7130c02-de8b-41fc-b54d-47c73db7cf9c
                Copyright © © The Author(s). 2017
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 9 May 2017
                Date accepted : 4 July 2017
                Categories
                Subject: Review
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                issue-copyright-statement © The Author(s) 2017

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