Clinical Translation of Microbiome Research in Alopecia Areata: A New Perspective?

Abstract

The continuous research advances in the microbiome field is changing clinicians’ points of view about the involvement of the microbiome in human health and disease, including autoimmune diseases such as alopecia areata (AA). Both gut and cutaneous dysbiosis have been considered to play roles in alopecia areata. A new approach is currently possible owing also to the use of omic techniques for studying the role of the microbiome in the disease by the deep understanding of microorganisms involved in the dysbiosis as well as of the pathways involved. These findings suggest the possibility to adopt a topical approach using either cosmetics or medical devices, to modulate or control, for example, the growth of overexpressed species using specific bacteriocins or postbiotics or with pH control. This will favour at the same time the growth of beneficial bacteria which, in turn, can impact positively both the structure of the scalp ecosystem on the host’s response to internal and external offenders. This approach, together with a “systemic” one, via oral supplementation, diet, or faecal transplantation, makes a reliable translation of microbiome research in clinical practice and should be taken into consideration every time alopecia areata is considered by a clinician.

Claudin‐3 is a novel intestinal integrity marker in patients with alopecia areata: Correlation with the disease severity

“…But many research show that alopecia areata is linked to systemic autoimmune activation, which implies markedly increased serum levels of Th1 (IL‐1, IL‐2, IL‐12, TNF‐, and IFN‐), Th2 (IL‐4, IL‐10, IL‐13, IL‐25, IL‐31), and Th17 cytokines (e.g., IL‐17A) 12 . The involvement of short‐chain fatty acids, primarily butyric acid, derived from microbial metabolism in the gut and the development of peripheral Treg cells has come to light, supporting the concept that there is a connection between AA and the gut microbiota 13 …”

“…Alopecia areata is an immunological disorder that causes non- Treg cells has come to light, supporting the concept that there is a connection between AA and the gut microbiota. 13 Claudins (CLDN) are tetraspan proteins consisting of a family of at least 24 members. It has been demonstrated that claudin-3 is expressed more strongly in distal than in proximal portions inside tubular tissues such as the intestine and nephron.…”