Host genome controls skin microbiota and inflammation

The human body contains more bacteria than human cells. Most of these bacteria comprise the normal gut and skin microbiota. Susceptibility to chronic inflammatory diseases is determined by immunogenetic and environmental risk factors that include resident microbial communities. Whether these differences are of primary etiological importance or secondary to the altered inflammatory environment remains largely unknown.

The inflammation cluster research groups led by Saleh Ibrahim of the University of Lübeck, and John Baines of the MPI and CAU, correlated the genomic variations of hundreds of mice that partially develop skin inflammatory diseases with skin microbiota. They showed evidence for host gene-microbiota interactions contributing to disease risk in a mouse model of autoantibody-induced inflammatory skin disease. Furthermore they identified genetic loci contributing to skin microbiota variability, susceptibility to skin inflammation and their overlap. The majority of the identified microbiotal communities are characterized by reduced abundance being associated with increased disease risk, providing evidence of a primary role in protection from disease.

These findings offer a promising potential for using those probiotic species for preventative and therapeutic treatment development. John Baines: "It appears that the skin flora is a phenotype that is partially controlled by the host genome variations. This in turn predisposes to the development of disease. The more we learn about these interactions, the more possibilities there will be for a better and more individualized treatment and prevention of skin inflammatory diseases.