Meet Your Microbiome
Last year I had the privilege of meeting Elling Ulvestad, a Norwegian microbiologist who is also a philosopher. He is a man of enormous warmth and energy, as well as having inexhaustible enthusiasm for his subject. He can soon convince anybody that the world is in great need of a philosophy that is properly informed by microbiology, and vice versa. Here are the kinds of facts that Professor Ulvestad has on the tip of his tongue. We carry 10 times as many bacterial cells around on our bodies as we do of our own cells (the disproportion is because microbes are very much smaller than mammalian cells). If you also count the bacteriophages that inhabit bacteria, the ratio of micro-organisms to human cells on each of us is probably more like 1000 : 1. Although we commonly regard bacteria as enemies, only around 100 species regularly infect human beings, while literally millions of others either ignore us or co-operate with us in ways that ensure our survival. We are, in other words, not isolated individuals but walking ecologies. Our lumbering, multicellular bodies act as unwitting landlords to a vast community of far more resilient lodgers who could happily move to alternative accommodation in someone else's gut or skin—and quite often do.
Ulvestad's view of human–microbial interaction—and his publications on the subject—go far beyond these numerical facts. He points out that micro-organisms have been the 'chief molecular innovators' of the biosphere. Evolutionary history has been built on their ability to project life to greater degrees of complexity. Micro-organisms are, quite literally, our ancestors, and they have incorporated themselves within our own genome. Forty-five per cent of the human genome consists of transposons—DNA sequences that can copy and move within chromosomes—of which around 8% are retrovirus-like. The DNA that regulates the interaction between the cell and its mitochondria is derived from bacteria. Mitochondria are of course themselves the descendants of formerly free-living bacteria. They have lost their ability to reproduce independently, but have made up for this by being shielded from immune destruction.
The development of our intestines, immune systems and even our brains is dependent on our bacterial cohabitants. Experimentally, mice raised with intestines free of germs display different behaviour from those which are allowed to acquire commensal bacteria. If the sterile mice are recolonised with bacteria while still in infancy, their behaviour becomes normal. If they are already adults, it does not. As Ulvestad argues 'Development impinges on evolution because it ties the organism up in a system of references to other living and non-living entities in between fertilisation and death'. Immune competence, he points out, should be understood as 'a relational property that transcends the boundary of the organism'. Thus, it should not surprise us if eradicating an obvious intestinal pathogen like Helicobacter pylori from the ecology may result in a backlash with a possibly increased incidence of asthma, diabetes and metabolic syndrome.
Introduction
Last year I had the privilege of meeting Elling Ulvestad, a Norwegian microbiologist who is also a philosopher. He is a man of enormous warmth and energy, as well as having inexhaustible enthusiasm for his subject. He can soon convince anybody that the world is in great need of a philosophy that is properly informed by microbiology, and vice versa. Here are the kinds of facts that Professor Ulvestad has on the tip of his tongue. We carry 10 times as many bacterial cells around on our bodies as we do of our own cells (the disproportion is because microbes are very much smaller than mammalian cells). If you also count the bacteriophages that inhabit bacteria, the ratio of micro-organisms to human cells on each of us is probably more like 1000 : 1. Although we commonly regard bacteria as enemies, only around 100 species regularly infect human beings, while literally millions of others either ignore us or co-operate with us in ways that ensure our survival. We are, in other words, not isolated individuals but walking ecologies. Our lumbering, multicellular bodies act as unwitting landlords to a vast community of far more resilient lodgers who could happily move to alternative accommodation in someone else's gut or skin—and quite often do.
Ulvestad's view of human–microbial interaction—and his publications on the subject—go far beyond these numerical facts. He points out that micro-organisms have been the 'chief molecular innovators' of the biosphere. Evolutionary history has been built on their ability to project life to greater degrees of complexity. Micro-organisms are, quite literally, our ancestors, and they have incorporated themselves within our own genome. Forty-five per cent of the human genome consists of transposons—DNA sequences that can copy and move within chromosomes—of which around 8% are retrovirus-like. The DNA that regulates the interaction between the cell and its mitochondria is derived from bacteria. Mitochondria are of course themselves the descendants of formerly free-living bacteria. They have lost their ability to reproduce independently, but have made up for this by being shielded from immune destruction.
The development of our intestines, immune systems and even our brains is dependent on our bacterial cohabitants. Experimentally, mice raised with intestines free of germs display different behaviour from those which are allowed to acquire commensal bacteria. If the sterile mice are recolonised with bacteria while still in infancy, their behaviour becomes normal. If they are already adults, it does not. As Ulvestad argues 'Development impinges on evolution because it ties the organism up in a system of references to other living and non-living entities in between fertilisation and death'. Immune competence, he points out, should be understood as 'a relational property that transcends the boundary of the organism'. Thus, it should not surprise us if eradicating an obvious intestinal pathogen like Helicobacter pylori from the ecology may result in a backlash with a possibly increased incidence of asthma, diabetes and metabolic syndrome.
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