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      Early-life disruption of amphibian microbiota decreases later-life resistance to parasites

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          Abstract

          Changes in the early-life microbiota of hosts might affect infectious disease risk throughout life, if such disruptions during formative times alter immune system development. Here, we test whether an early-life disruption of host-associated microbiota affects later-life resistance to infections by manipulating the microbiota of tadpoles and challenging them with parasitic gut worms as adults. We find that tadpole bacterial diversity is negatively correlated with parasite establishment in adult frogs: adult frogs that had reduced bacterial diversity as tadpoles have three times more worms than adults without their microbiota manipulated as tadpoles. In contrast, adult bacterial diversity during parasite exposure is not correlated with parasite establishment in adult frogs. Thus, in this experimental setup, an early-life disruption of the microbiota has lasting reductions on host resistance to infections, which is possibly mediated by its effects on immune system development. Our results support the idea that preventing early-life disruption of host-associated microbiota might confer protection against diseases later in life.

          Abstract

          Early-life microbiota alterations can affect infection susceptibility later in life, in animal models. Here, Knutie et al. show that manipulating the microbiota of tadpoles leads to increased susceptibility to parasitic infection in adult frogs, in the absence of substantial changes in the adults’ microbiota.

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          The intestinal microbiome is a signalling hub that integrates environmental inputs, such as diet, with genetic and immune signals to affect the host's metabolism, immunity and response to infection. The haematopoietic and non-haematopoietic cells of the innate immune system are located strategically at the host-microbiome interface. These cells have the ability to sense microorganisms or their metabolic products and to translate the signals into host physiological responses and the regulation of microbial ecology. Aberrations in the communication between the innate immune system and the gut microbiota might contribute to complex diseases.
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                Author and article information

                Contributors
                saknutie@gmail.com
                Journal
                Nat Commun
                Nat Commun
                Nature Communications
                Nature Publishing Group UK (London )
                2041-1723
                20 July 2017
                20 July 2017
                2017
                : 8
                : 86
                Affiliations
                [1 ]ISNI 0000 0001 2353 285X, GRID grid.170693.a, Department of Integrative Biology, , University of South Florida, ; Tampa, FL 33620 USA
                [2 ]ISNI 0000 0001 2264 7217, GRID grid.152326.1, Department of Biological Sciences, , Vanderbilt University, ; 465 21st Ave South, Nashville, TN 37235 USA
                [3 ]ISNI 0000 0001 0860 4915, GRID grid.63054.34, Department of Ecology and Evolutionary Biology, , University of Connecticut, ; Storrs, CT 06269 USA
                [4 ]ISNI 0000 0004 1936 9000, GRID grid.21925.3d, Department of Biological Sciences, , University of Pittsburgh, ; Pittsburgh, PA 15260 USA
                Author information
                http://orcid.org/0000-0001-6423-9561
                Article
                119
                10.1038/s41467-017-00119-0
                5519754
                28729558
                c0a1d9d0-a577-47b3-8bd7-257b1c2d5e91
                © The Author(s) 2017

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 14 October 2016
                : 2 June 2017
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