Characterization of the skin microbiota in bullous pemphigoid patients and controls reveals novel microbial indicators of disease

Identification of gut microbiota dysbiosis in bullous pemphigoid under different disease activity

“…By bioinformatics analysis, we observed a trend of increased alpha diversity in BP patients compared with HC. This contradicts previous studies on BP skin microbiota 15 or other inflammatory skin diseases, such as psoriasis 29 . Previous studies have shown that reduced diversity in microbiota is due to the loss of protective microbiota, but our data suggest that an increase in pathogenic bacteria may be involved in BP, supporting the hypothesis that gut microbiome dysbiosis with an increased proportion of potentially pathogenic bacteria may exist in BP patients.…”

“…14 In BP patients, the skin microbiota composition has been proven to be substantially different from the healthy people and a novel indicator of disease. 15 The GM in BP patients has rarely been examined. Also, the altered GM composition may be related to treatment effect.…”

“…In previous study, other autoimmune bullous diseases such as mucous membrane pemphigoid (MMP) have been investigated and GM dysbiosis was observed in MMP patients 14 . In BP patients, the skin microbiota composition has been proven to be substantially different from the healthy people and a novel indicator of disease 15 . The GM in BP patients has rarely been examined.…”

Interleukin‐36 cytokines are overexpressed in the skin and sera of patients with bullous pemphigoid

“…In a recent BP mouse model obtained by genetic deletion of the NC14A domain (the mouse correspondent of NC16A), skin lesions showed increased levels of IL‐17 and IL‐17‐associated cytokines, including IL‐36α/γ, which decreased after IL‐17 inhibition, 24 suggesting a link between IL‐17 signalling and the release of IL‐36. However, additional factors might also contribute to IL‐36 production and release in BP: skin injury, a known external trigger of BP, is known to induce the release of IL‐36γ 25,26 ; moreover, S. aureus , an inflammation‐promoting species which is abundant in the skin lesions of BP patients, 27 is known to trigger the release of IL‐36 α 28 …”

“…In a recent BP mouse model obtained by genetic deletion of the NC14A domain (the mouse correspondent of NC16A), skin lesions showed increased levels of IL-17 and IL-17-associated cytokines, including IL-36α/γ, which decreased after IL-17 inhibition, 24 suggesting a link between IL-17 signalling and the release of IL-36. However, additional factors might also contribute to IL-36 production and release in BP:skin injury, a known external trigger of BP, is known to induce the release of IL-36γ25,26 ; moreover, S. aureus, an inflammation-promoting species which is abundant in the skin lesions of BP patients,27 is known to trigger the release of IL-36 α 28. All IL-36 isoforms are released in a less biologically active precursor forms, which requires processing and activation byF I G U R E 1 Expression of IL-36 molecules in the skin of patients with bullous pemphigoid (BP): mRNA expression of IL-36α (A), IL-36β (B), IL-36γ (C), IL-36Ra (D) and IL-38 (E) was assessed in the skin of patients with BP, psoriasis (Pso) and healthy control (HC) by qPCR and data were normalized to HPRT1 housekeeping mRNA levels.…”