Genome-wide mapping of gene–microbiota interactions in susceptibility to autoimmune skin blistering

Girish Srinivas, Steffen Möller, Jun Wang, Sven Künzel, Detlef Zillikens, John F. Baines () and Saleh M. Ibrahim
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Girish Srinivas: Max Planck Institute for Evolutionary Biology
Steffen Möller: University of Lübeck
Jun Wang: Max Planck Institute for Evolutionary Biology
Sven Künzel: Max Planck Institute for Evolutionary Biology
Detlef Zillikens: University of Lübeck
John F. Baines: Max Planck Institute for Evolutionary Biology
Saleh M. Ibrahim: University of Lübeck

Nature Communications, 2013, vol. 4, issue 1, 1-7

Abstract: Abstract Susceptibility to chronic inflammatory diseases is determined by immunogenetic and environmental risk factors. Resident microbial communities often differ between healthy and diseased states, but whether these differences are of primary aetiological importance or secondary to the altered inflammatory environment remains largely unknown. Here we provide evidence for host gene–microbiota interactions contributing to disease risk in a mouse model of epidermolysis bullosa acquisita, an autoantibody-induced inflammatory skin disease. Using an advanced intercross, we identify genetic loci contributing to skin microbiota variability, susceptibility to skin blistering and their overlap. Furthermore, by treating bacterial species abundances as covariates with disease we reveal a novel disease locus. The majority of the identified covariate taxa are characterized by reduced abundance being associated with increased disease risk, providing evidence of a primary role in protection from disease. Further characterization of these putative probiotic species or species assemblages offers promising potential for preventative and therapeutic treatment development.

Date: 2013
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DOI: 10.1038/ncomms3462

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