As our knowledge of the human microbiome expands, so too does our realisation of its fundamental contributions to health and disease. Such are the benefits to us, the host, of our microbial fellow travellers that some have proposed that the gut microbiota be regarded as an ‘organ’ integral to the homoeostasis of the entire organism.
This proposal is amply supported, first, by ever-accumulating evidence of a fundamental role for the microbiota in the genesis of immune responses, not just in the gut, but throughout the body and, secondly, by the recognition of its substantial contribution to a variety of metabolic processes.[2, 3] Sharing the limelight with the microbiome as one of the ‘hottest’ areas of biomedical research has been inflammation, through the recognition of contributions from inflammatory processes to disease states as diverse as atherosclerosis, depression, Alzheimer's disease, cancer, obesity and the metabolic syndrome.
Given that so many of these disorders are age-related in prevalence, a unifying hypothesis, ‘inflamm-ageing’, has emerged, which proposes that a common biological factor could be responsible for an age-related rise in inflammatory disorders. That the microbiota could be this factor (or, at the very least, one of many contributory factors) is suggested by the landmark study of Claesson and colleagues who demonstrated an association between gut microbial diversity, inflammatory markers and health status in their population of elderly subjects.
The obvious question that emanates from all of this is: can we intervene to reverse or prevent ‘inflamm-ageing’ and its clinical consequences? There is already considerable evidence, albeit from studies of association rather than dietary intervention, that diet and the microbiota are inextricably linked  and there is some data to extend this linkage to inflammatory status.
Macfarlane and colleagues now address this issue in an intervention study where they administered a synbiotic product for 4 weeks to 43 subjects aged between 65 and 90 and demonstrated significant changes in the relative preponderance of various microbial species (most notably, an increase in the numbers of Bifidobacteria spp.) and an associated increase in butyrate production and reduction in the important pro-inflammatory cytokine, tumour necrosis factor alpha.
These are intriguing findings, which support the linkage between diet (in this instance, a prebiotic), the microbiota, metabolism and inflammation. That this strategy might be relevant to human disease is illustrated by recent data demonstrating the ability of a probiotic to reduce inflammatory markers in a number of inflammatory disorders.