A key genetic factor for fucosyllactose utilization affects infant gut microbiota development

Takahiro Matsuki (), Kana Yahagi, Hiroshi Mori, Hoshitaka Matsumoto, Taeko Hara, Saya Tajima, Eishin Ogawa, Hiroko Kodama, Kazuya Yamamoto, Takuji Yamada, Satoshi Matsumoto and Ken Kurokawa
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Takahiro Matsuki: Yakult Central Institute
Kana Yahagi: Yakult Central Institute
Hiroshi Mori: Tokyo Institute of Technology
Hoshitaka Matsumoto: Yakult Central Institute
Taeko Hara: Yakult Central Institute
Saya Tajima: Yakult Central Institute
Eishin Ogawa: Teikyo University School of Medicine
Hiroko Kodama: Teikyo University School of Medicine
Kazuya Yamamoto: Tokyo Institute of Technology
Takuji Yamada: Tokyo Institute of Technology
Satoshi Matsumoto: Yakult Central Institute
Ken Kurokawa: Tokyo Institute of Technology

Nature Communications, 2016, vol. 7, issue 1, 1-12

Abstract: Abstract Recent studies have demonstrated that gut microbiota development influences infants’ health and subsequent host physiology. However, the factors shaping the development of the microbiota remain poorly understood, and the mechanisms through which these factors affect gut metabolite profiles have not been extensively investigated. Here we analyse gut microbiota development of 27 infants during the first month of life. We find three distinct clusters that transition towards Bifidobacteriaceae-dominant microbiota. We observe considerable differences in human milk oligosaccharide utilization among infant bifidobacteria. Colonization of fucosyllactose (FL)-utilizing bifidobacteria is associated with altered metabolite profiles and microbiota compositions, which have been previously shown to affect infant health. Genome analysis of infants’ bifidobacteria reveals an ABC transporter as a key genetic factor for FL utilization. Thus, the ability of bifidobacteria to utilize FL and the presence of FL in breast milk may affect the development of the gut microbiota in infants, and might ultimately have therapeutic implications.

Date: 2016
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DOI: 10.1038/ncomms11939

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