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There is a developing appreciation of the abundance and diversity of the trillions of micro-organisms that live on and within us,1 ,2 and how they influence human health and disease.3 Outnumbering human cells in our bodies by 10:1, and their genes outnumbering ours by 100:1,4 bacteria in the gastrointestinal (GI) tract have the potential to significantly modulate human metabolism.5 Previous studies of the microbiota (all the microbes in a given environment) have been hampered by the difficulties of culturing complex samples containing fastidious or unculturable organisms, resulting in inaccurate depictions of microbial communities. Microbiota studies have now progressed to identifying organisms by their DNA sequence. A particular focus has been on the bacterial component, exploiting sequence variation in the ubiquitous 16S rRNA gene. By careful choice of primers hybridising to highly conserved domains within 16S rRNA,6 a sufficiently large and variable region of this gene can be amplified and sequenced for organisms to be identified at least at genus level, without the bias arising from the need for culture. Utilising next-generation sequencing, which allows millions of sequencing reactions to be performed in parallel, we can determine in quantitative fashion, as never before, the composition of complex bacterial communities,7 such as exist in faecal samples, a pragmatic surrogate for the microbiota of the GI tract mucosal surface.8
Two large international initiatives, The Human Microbiome Project (HMP)9 and Metagenomics of the Human Intestinal Tract (MetaHIT),10 have used this approach to characterise the adult human microbiota at different body sites in health and disease. There is a burgeoning interest in the neonatal GI microbiota, and its association with diseases of prematurity,11 normal child development4 and future health.12 Our group is conducting a longitudinal prospective study assessing the importance of …
KS, EP and AGS contributed equally
Contributors All authors contributed to the text. KS, EP, AGS and SK were involved in the critical revision of the manuscript, and SK approved the final version.
Funding KS is funded by a Doctoral Research Fellowship award from the National Institute for Health Research (Grant code P35969). MB was a Lister Institute summer student. NeoM and our other projects characterising the neonatal GI microbiota have been generously funded by The Winnicott Foundation (P26859) and Meningitis UK (P35505).
Competing interests None.
Provenance and peer review Commissioned; externally peer reviewed.
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