Commentary

This interesting and innovative article addresses possible peculiarities of the microbiota present in the miniaturized hair follicle when compared to the terminal hair follicle as well as to the control patients without androgenetic alopecia. This may be a relevant step to expand the therapeutic possibilities in this disease, which is as prevalent as it is impacting on the self-esteem of several affected patients.

Introduction

Androgenetic alopecia (AGA) is the most common form of hair loss in men and is caused by genetic predisposition and abnormality of androgen activity. It is a chronic condition characterized by progressive miniaturization of scalp hair. Some publications report that the pathogenesis of AGA is multifactorial and goes beyond the hormonal and genetic component, suggesting the participation of the microbiome in the onset of the disease. However, the role of microflora during hair loss remains to be understood This article aims to analyze the microbiome of hair follicles from hair losspatients and the healthy. This is the first study characterizing microbiome in the middle and lower hair compartment in healthy and AGA patients to understand the possible link with AGA progression.

Methods and Results

Using 16S shotgun rRNA sequencing, the authors determined the microbiome in the middle and lower portions of occipital and vertex hair follicles from 20 patients presenting with AGA and 10 healthy controls. Distinct microbial population were found in the middle and lower compartment of hair follicles. Middle hair compartment was predominated by Burkholderia spp. and less diverse, while higher bacterial diversity was observed in the lower hair portion. Occipital and vertex hair follicles did not show significant differences. In hair loss patients, miniaturized vertex hair houses elevated Propionibacterium acnes in the middle and lower compartments while non-miniaturized hair of other regions were comparable to the healthy.

Discussion

Little is known about the hair follicle micro-environment. It has long been speculated that P. acnes is involved in AGA pathogenesis. P. acnes is a common opportunistic pathogen found on the skin surface and is prevalent in the hair follicle and the associated pilosebaceous unit. P. acnes predominance is also identified in non-lesioned scalp of patients with seborrheic dermatitis, providing further support for the development in sebaceous gland hyperplasia in AGA may attract the proliferation of P. acnes for lipids and fatty acids are its main nutrient sources. It has been reported that P. acnes and residential microflora of the hair and skin can elicit innate immune responses through toll like receptor 2 and upregulation of anti-microbial peptides including beta-defensin. This microinflammation could be cause or consequence of the hair miniaturization process. Therefore, increased abundance of P. acnes in miniaturized hair follicles could be associated to elevated immune response gene expression in the hair follicle.
Evidence of micro-inflammation such as perifollicular inflammatory infiltration, prostaglandin and cytokine elevation have been observed in hair follicles of AGA patients and is suggested to cause hair miniaturization. This paper brings data reinforcing the role of P. acnes as a contributing factor for micro-inflammation in hair loss patients.

Conclusion

The present article provided novel insights reporting distinct microbial population in the middle and lower portion of the hair follicle. As mentioned in result section, Burkholderia genera predominates in the middle portion while higher microbial diversity was observed in the lower portion. In AGA patients, miniaturized patient vertex hair houses elevated P. acnes while hair from other regions were comparable. This study improves the understanding of the role of the microbiome in the pathogenesis of androgenetic alopecia.