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.
| Original language | English |
|---|---|
| Journal | Experimental Dermatology |
| Volume | 26 |
| Issue number | 12 |
| Pages (from-to) | 1221-1227 |
| Number of pages | 7 |
| ISSN | 0906-6705 |
| DOIs | |
| Publication status | Published - 01.12.2017 |
Funding
German Science Foundation (DFG); Excellence Cluster 306/2; German Centre for Infection Research (DZIF) We would like to thank M. Belheouane and P. Rausch for fruitful discussions and M. Baden for the help in patients’ recruitment. This work was supported by the German Science Foundation (DFG) Clinical Research Unit 303 “Pemphigoid Diseases—Molecular Pathways and their Therapeutic Potential” subprojects BA 2863/6-1 (JFB), SCHM 1686/6-1 (ES) and IB 24/10-1 (SMI) and by infrastructural funds from Excellence Cluster 306/2 “Inflammation at Interfaces”. EAL was supported by the German Centre for Infection Research (DZIF).