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      Longitudinal Changes in the Gut Microbiome of Infants on Total Parenteral Nutrition

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          Abstract

          Background:

          Animal studies suggest that total parenteral nutrition (TPN) may alter bacterial colonization of the intestinal tract and contribute to complications. Progressive changes in gut microbiome of infants receiving TPN are not well understood.

          Methods:

          Infants with and without TPN/soy lipid were enrolled in a prospective, longitudinal study. Weekly fecal samples were obtained for the first 4 weeks of life. High throughput pyrosequencing of 16S rDNA was used for compositional analysis of the gut microbiome.

          Results:

          47 infants were eligible for analyses, 25 infants received TPN and 22 infants did not (control). Although similar between TPN and control groups in the first week, fecal bacterial alpha diversity was significantly lower in the TPN group compared to controls at week 4 (Shannon index 1.0 vs 1.5, P-value = 0.03). The TPN group had significantly lower Bacteroidetes and higher Verrucomicrobia abundance compared to controls (P-values <0.05), and these differences became more pronounced over time. At the genus level, TPN was associated with lower abundance of Bacteroides and Bifidobacterium in all weeks.

          Conclusions:

          TPN is associated with significant loss of biodiversity and alterations in the pattern of gut microbial colonization of infants over time. TPN-associated dysbiosis may predispose infants to adverse NICU outcomes.

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          Most cited references28

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          A microbial symbiosis factor prevents intestinal inflammatory disease.

          Humans are colonized by multitudes of commensal organisms representing members of five of the six kingdoms of life; however, our gastrointestinal tract provides residence to both beneficial and potentially pathogenic microorganisms. Imbalances in the composition of the bacterial microbiota, known as dysbiosis, are postulated to be a major factor in human disorders such as inflammatory bowel disease. We report here that the prominent human symbiont Bacteroides fragilis protects animals from experimental colitis induced by Helicobacter hepaticus, a commensal bacterium with pathogenic potential. This beneficial activity requires a single microbial molecule (polysaccharide A, PSA). In animals harbouring B. fragilis not expressing PSA, H. hepaticus colonization leads to disease and pro-inflammatory cytokine production in colonic tissues. Purified PSA administered to animals is required to suppress pro-inflammatory interleukin-17 production by intestinal immune cells and also inhibits in vitro reactions in cell cultures. Furthermore, PSA protects from inflammatory disease through a functional requirement for interleukin-10-producing CD4+ T cells. These results show that molecules of the bacterial microbiota can mediate the critical balance between health and disease. Harnessing the immunomodulatory capacity of symbiosis factors such as PSA might potentially provide therapeutics for human inflammatory disorders on the basis of entirely novel biological principles.
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            Microbes inside--from diversity to function: the case of Akkermansia.

            The human intestinal tract is colonized by a myriad of microbes that have developed intimate interactions with the host. In healthy individuals, this complex ecosystem remains stable and resilient to stressors. There is significant attention on the understanding of the composition and function of this intestinal microbiota in health and disease. Current developments in metaomics and systems biology approaches allow to probe the functional potential and activity of the intestinal microbiota. However, all these approaches inherently suffer from the fact that the information on macromolecules (DNA, RNA and protein) is collected at the ecosystem level. Similarly, all physiological and other information collected from isolated strains relates to pure cultures grown in vitro or in gnotobiotic systems. It is essential to integrate these two worlds of predominantly chemistry and biology by linking the molecules to the cells. Here, we will address the integration of omics- and culture-based approaches with the complexity of the human intestinal microbiota in mind and the mucus-degrading bacteria Akkermansia spp. as a paradigm.
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              Is Open Access

              Microbiota fingerprints lose individually identifying features over time

              Background Humans host individually unique skin microbiota, suggesting that microbiota traces transferred from skin to surfaces could serve as forensic markers analogous to fingerprints. While it is known that individuals leave identifiable microbiota traces on surfaces, it is not clear for how long these traces persist. Moreover, as skin and surface microbiota change with time, even persistent traces may lose their forensic potential as they would cease to resemble the microbiota of the person who left them. We followed skin and surface microbiota within households for four seasons to determine whether accurate microbiota-based matching of individuals to their households could be achieved across long time delays. Results While household surface microbiota traces could be matched to the correct occupant or occupants with 67% accuracy, accuracy decreased substantially when skin and surface samples were collected in different seasons, and particularly when surface samples were collected long after skin samples. Most OTUs persisted on skin or surfaces for less than one season, indicating that OTU loss was the major cause of decreased matching accuracy. OTUs that were more useful for individual identification persisted for less time and were less likely to be deposited from skin to surface, suggesting a trade-off between the longevity and identifying value of microbiota traces. Conclusions While microbiota traces have potential forensic value, unlike fingerprints they are not static and may degrade in a way that preferentially erases features useful in identifying individuals. Electronic supplementary material The online version of this article (doi:10.1186/s40168-016-0209-7) contains supplementary material, which is available to authorized users.
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                Author and article information

                Journal
                0100714
                6400
                Pediatr Res
                Pediatr. Res.
                Pediatric research
                0031-3998
                1530-0447
                1 April 2019
                09 April 2019
                July 2019
                09 October 2019
                : 86
                : 1
                : 107-114
                Affiliations
                [1 ]Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI
                [2 ]Center for Microbiome Research, Medical College of Wisconsin, Milwaukee, WI
                Author notes

                Author Contributions:

                Each author has met the requirements for authorship. Substantial contributions to conception and design, acquisition of data, or analysis and interpretation of data were made by AF Dahlgren, A Pan, V Lam, KC Gouthro, PM Simpson, NH Salzman, and TH Nghiem-Rao. The first draft of the manuscript was written by TH Nghiem-Rao, and all authors contributed to revising the manuscript critically for important intellectual content. Each author has seen and approved the submission of this manuscript.

                [* ] Corresponding author: T. Hang Nghiem-Rao, MD, Medical College of Wisconsin, PO Box 1997, 999 N. 92 Street, Milwaukee, WI 53226, USA, Phone: 414-266-6820, Fax: 414-266-6979, hnghiem@ 123456mcw.edu
                Article
                NIHMS1525951
                10.1038/s41390-019-0391-y
                6594895
                30965357
                a4fc06fc-a82e-47c6-b1c7-be606f66d962

                Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

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                Pediatrics
                Pediatrics

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