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A distinct cutaneous microbiota profile in autoimmune bullous disease patients

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Künstner,  Axel
Guest Group Evolutionary Genomics, Max Planck Institute for Evolutionary Biology, Max Planck Society;

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Baines,  John F.
Guest Group Evolutionary Genomics, Max Planck Institute for Evolutionary Biology, Max Planck Society;

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Miodovnik, M., Künstner, A., Langan, E. A., Zillikens, D., Gläser, R., Sprecher, E., et al. (2017). A distinct cutaneous microbiota profile in autoimmune bullous disease patients. Experimental Dermatology: an International Journal for Rapid Publication of Short Reports in Experimental Dermatology, 1221-1227. doi:10.1111/exd.13357.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002E-5F0C-7
Abstract
Bullous pemphigoid (BP) is the most common autoimmune blistering disease in Europe. As both the incidence of the disease and the relative proportion of the elderly population continue to rise, it represents a significant medical burden. Whereas some progress has been achieved in defining genetic risk factors for autoimmune blistering diseases, no environmental agent has been conclusively identified. Emerging evidence suggests that host immunity may influence the skin microbiota, while the latter modulates cutaneous immunity. Nevertheless, the relationship between skin microbial communities and autoimmune bullous disease has yet to be studied in humans. Here, we aim to characterise and compare the skin microbiome of patients with BP and healthy, age-matched controls at numerous body sites. Similar to what has been shown in healthy controls, the composition of skin microbiota in patients with BP appears to be very divergent and site specific. Microbial phylum abundances differ between perilesional sites of patients with BP and the same anatomic locations of control patients. A distinct cutaneous microbiota profile, which correlates with BP, further strengthens the significance of commensal-host interaction on our immune system. Moreover, these results raise the possibility that the cutaneous microbiome may contribute to the pathogenesis of BP, with important implications for the treatment of this disease. © 2017 John Wiley Sons Ltd.