Open this publication in new window or tab >>BGI-Shenzhen, Shenzhen, China.
The Wallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
BGI-Shenzhen, Shenzhen, China.
BGI-Shenzhen, Shenzhen, China.
BGI-Shenzhen, Shenzhen, China.
BGI-Shenzhen, Shenzhen, China.
The Wallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
BGI-Shenzhen, Shenzhen, China.
BGI-Shenzhen, Shenzhen, China.
BGI-Shenzhen, Shenzhen, China.
BGI-Shenzhen, Shenzhen, China & Princess Al Jawhara Albrahim Center of Excellence in the Research of Hereditary Disorders, King Abdulaziz University, Saudi Arabia.
BGI-Shenzhen, Shenzhen, China.
The Wallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
Department of Biology, University of Copenhagen, Copenhagen, Denmark.
Department of Biology, University of Copenhagen, Copenhagen, Denmark.
The Wallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
BGI-Shenzhen, Shenzhen, China.
Göteborg Paediatric Growth Research Center, Department of Paediatrics, the University of Gothenburg, Queen Silvia Children’s Hospital, Gothenburg & Research and Development Center Spenshult, Oskarström, Sweden.
BGI-Shenzhen, Shenzhen, China.
Department of Biology, University of Copenhagen, Copenhagen, Denmark & National Institute of Nutrition and Seafood Research, Bergen, Norway.
BGI-Shenzhen, Shenzhen, China & Department of Biology, University of Copenhagen, Copenhagen, Denmark.
Göteborg Paediatric Growth Research Center, Department of Paediatrics, the University of Gothenburg, Queen Silvia Children’s Hospital, Gothenburg & .
BGI-Shenzhen, Shenzhen, China, Department of Biology, University of Copenhagen, Copenhagen, Denmark, Princess Al Jawhara Albrahim Center of Excellence in the Research of Hereditary Disorders, King Abdulaziz University, Saudi Arabia, Macau University of Science and Technology, Avenida Wai long, Taipa, China & Department of Medicine and State Key Laboratory of Pharmaceutical Biotechnology, University of Hong Kong, Hong Kong.
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2015 (English)In: Cell Host and Microbe, ISSN 1931-3128, E-ISSN 1934-6069, Vol. 17, no 5, p. 690-703Article in journal (Refereed) Published
Abstract [en]
The gut microbiota is central to human health, but its establishment in early life has not been quantitatively and functionally examined. Applying metagenomic analysis on fecal samples from a large cohort of Swedish infants and their mothers, we characterized the gut microbiome during the first year of life and assessed the impact of mode of delivery and feeding on its establishment. In contrast to vaginally delivered infants, the gut microbiota of infants delivered by C-section showed significantly less resemblance to their mothers. Nutrition had a major impact on early microbiota composition and function, with cessation of breast-feeding, rather than introduction of solid food, being required for maturation into an adult-like microbiota. Microbiota composition and ecological network had distinctive features at each sampled stage, in accordance with functional maturation of the microbiome. Our findings establish a framework for understanding the interplay between the gut microbiome and the human body in early life. © 2015 Elsevier Inc.
Place, publisher, year, edition, pages
Cambridge: Cell Press, 2015
National Category
Pediatrics
Identifiers
urn:nbn:se:hh:diva-29962 (URN)10.1016/j.chom.2015.04.004 (DOI)000356101500020 ()25974306 (PubMedID)2-s2.0-84929297936 (Scopus ID)
Funder
Knut and Alice Wallenberg FoundationSwedish Research CouncilNovo Nordisk
2015-12-072015-12-072025-10-01Bibliographically approved