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Br J Dermatol. 2016 Oct;175 Suppl 2:13-18. doi: 10.1111/bjd.14907.

The role of skin and gut microbiota in the development of atopic eczema.

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Division of Asthma, Allergy and Lung Biology, Department of Paediatric Allergy, King's College London, London, U.K.
Children's Allergies Department, Guy's and St Thomas' NHS Foundation Trust, St Thomas' Hospital, Westminster Bridge Road, Lambeth, SE1 7EH, U.K.
Unit for Population-Based Dermatology Research, St John's Institute of Dermatology, Division of Genetics and Molecular Medicine, King's College London and Guy's and St Thomas' Hospital NHS Foundation Trust, London, U.K.


Conventional culture-based studies have suggested that a reduction in microbial exposure in early life predisposes to atopic eczema and allergies. However, molecular microbiological methods have shown that conventional culture fails to grow around 80% of the bacterial flora. More recent work reviewed in this paper has employed next generation sequencing to study the influence of the gut and skin microbiota, both with regard to the risk of developing atopic eczema but also the role of pathogenic and commensal bacteria in established disease. Birth cohorts investigating the gastrointestinal tract reported reduced faecal microbiota diversity among those who later developed atopic eczema, using gel electrophoresis, real-time PCR or 16S ribosomal RNA gene pyrosequencing. However, the inverse association with reduced faecal bacterial diversity was not confirmed in cross-sectional studies among patients with established atopic eczema. Only two studies investigated the cutaneous microbiota in a longitudinal study design and both were unable to provide evidence that Staphylococcus aureus colonisation precedes the development of atopic eczema. Next generation sequencing has confirmed the cross-sectional association between atopic eczema and S. aureus colonisation. The two studies that used this approach have also shown that disease flares are associated with a significant fall in skin microbiota diversity and an increase in the relative abundance of both S. aureus and epidermidis. Interestingly, S. aureus elimination does not appear to be the main reason why atopic eczema improves after a flare and antimicrobial and anti-inflammatory therapy enhances bacterial diversity. Further, well-phenotyped birth cohorts that take key confounders, such as antibiotic exposure, into account are required.


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