Format

Send to

Choose Destination
Lancet. 2017 Jul 29;390(10093):521-530. doi: 10.1016/S0140-6736(17)30566-4. Epub 2017 Jul 27.

Evolution, human-microbe interactions, and life history plasticity.

Author information

1
Centre for Clinical Microbiology, Department of Infection, UCL (University College London), London, UK. Electronic address: g.rook@ucl.ac.uk.
2
The Wallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
3
Department of Biology, Emory University, Atlanta, GA, USA.
4
Pacific Biosciences Research Center, University of Hawaii at Manoa, Hawaii, HI, USA.
5
Department of Zoology, University of Oxford, South Parks Road, Oxford, UK.

Abstract

A bacterium was once a component of the ancestor of all eukaryotic cells, and much of the human genome originated in microorganisms. Today, all vertebrates harbour large communities of microorganisms (microbiota), particularly in the gut, and at least 20% of the small molecules in human blood are products of the microbiota. Changing human lifestyles and medical practices are disturbing the content and diversity of the microbiota, while simultaneously reducing our exposures to the so-called old infections and to organisms from the natural environment with which human beings co-evolved. Meanwhile, population growth is increasing the exposure of human beings to novel pathogens, particularly the crowd infections that were not part of our evolutionary history. Thus some microbes have co-evolved with human beings and play crucial roles in our physiology and metabolism, whereas others are entirely intrusive. Human metabolism is therefore a tug-of-war between managing beneficial microbes, excluding detrimental ones, and channelling as much energy as is available into other essential functions (eg, growth, maintenance, reproduction). This tug-of-war shapes the passage of each individual through life history decision nodes (eg, how fast to grow, when to mature, and how long to live).

PMID:
28792414
DOI:
10.1016/S0140-6736(17)30566-4
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center