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Abstract
Human skin serves as the first line of defense against pathogenic bacteria, while
also providing a home to billions of symbiotic bacteria. By sequencing the DNA of
bacteria collected from the skin of humans and mouse models of human disease, we investigated
how these bacteria contribute to health and, conversely, how changes in the bacterial
community structure might contribute to chronic skin disorders.
Our analysis of 16S ribosomal RNA gene sequences obtained from 20 distinct skin sites
of healthy humans revealed that physiologically comparable sites harbor similar bacterial
communities and provides a baseline for studies that examine the role of bacterial
communities in disease states and the microbial inter-dependencies required to maintain
healthy skin. We explored the selective shift in the microbiota observed in skin disorders
commonly treated with antimicrobial agents such as eczema and diabetic wound healing.
For example, we show that a longitudinal selective shift in wound microbiota coincides
with impaired healing in diabetic mice. We demonstrate a parallel shift in longitudinal
gene expression that occurs in a cluster of genes related to the immune response.
Furthermore, we establish a correlation between relative abundance of Staphylococcus
spp. and the expression of cutaneous defense response genes. These data demonstrate
that integrating two types of global data sets lends a better understanding to the
dynamics governing host-microbe interactions. Clinical management of these disorders
requires better biomarkers to realize the therapeutic potential of manipulating the
microbiome. Targeted therapies to maintain healthy skin might require not only inhibiting
the growth of pathogenic bacteria, but also promoting the growth of symbiotic bacteria.
Microbiome studies show the power of bridging genomics and clinical medicine to gain
valuable insight into the human body as a complex super-organism.