An update on the microbiology, immunology and genetics of seborrheic dermatitis

Abstract

The underlying mechanism of seborrheic dermatitis (SD) is poorly understood but major scientific progress has been made in recent years related to microbiology, immunology and genetics. In light of this, the major goal of this article was to summarize the most recent articles on SD, specifically related to underlying pathophysiology. SD results from Malassezia hydrolysation of free fatty acids with activation of the immune system by the way of pattern recognition receptors, inflammasome, IL-1β and NF-kB. M. restricta and M. globosa are likely the most virulent subspecies, producing large quantities of irritating oleic acids, leading to IL-8 and IL-17 activation. IL-17 and IL-4 might play a big role in pathogenesis, but this needs to be further studied using novel biologics. No clear genetic predisposition has been established; however, recent studies implicated certain increased-risk human leucocyte antigen (HLA) alleles, such as A*32, DQB1*05 and DRB1*01 as well as possible associations with psoriasis and atopic dermatitis (AD) through the LCE3 gene cluster while SD, and SD-like syndromes, shares genetic mutations that appear to impair the ability of the immune system to restrict Malassezia growth, partially due to complement system dysfunction. A paucity of studies exists looking at the relationship between SD and systemic disease. In HIV, SD is thought to be secondary to a combination of immune dysregulation and disruption in skin microbiota with unhindered Malassezia proliferation. In Parkinson's disease, SD is most likely secondary to parasympathetic hyperactivity with increased sebum production as well as facial immobility which leads to sebum accumulation. K E Y W O R D Sinflammasome, Malassezia, sebaceous glands, seborrheic dermatitis, systemic disease While the order of events is unclear regarding the pathophysiology of SD, it is agreed upon by most sources that the three main prerequisites are as follows: Malassezia colonization, lipid secretion by sebaceous glands and an underlying immune system susceptibility. [1,5,7,38] The pathogenesis can be categorized into five different phases.

Parkinson's disease and skin

“…Melanoma, seborrheic dermatitis (SD), sweating dysfunction, and bullous pemphigoid (BP) are overrepresented in PD [4][5][6]. Some skin disorders such as SD [7] and sweating dysfunction [8] may in part be due to peripheral autonomic dysfunction and can predate onset of PD motor symptoms. Melanoma [9] and BP [10], which seem to have a more complex relation to PD, often develop years after the diagnosis of PD has been established.…”

The Evaluation of 2D/4D Finger Ratios in Seborrheic Dermatitis Cases

“…One of the most important of these factors is the role of androgens on the sebaceous glands. The causes such as higher prevalence in male gender, predilection regions where the sebum production is more intensive, and the disease seen after puberty are indicators that androgens play a role in the etiopathogenesis of seborrheic dermatitis (8). Again, in some patients, seborrheic dermatitis regress after adrenalectomy or after anti-androgen therapy.…”

Potential role of the skin microbiota in Inflammatory skin diseases

“…Over the past decade, with the advancement and improvement 11 atopic dermatitis, 12 psoriasis, 13 and acne. 14 The emergence of new technology enables researchers to have a more comprehensive understanding and analysis of skin microbiota.…”

“…Over the past decade, with the advancement and improvement of next‐generation sequencing platforms, researchers can analyze the composition of various microorganisms in microbiota by high‐throughput sequencing 9 . At present, researchers have applied 16S rRNA, ITS gene sequencing, and metagenome sequencing to analyze the characteristics of skin microbiota in skin diseases such as seborrheic dermatitis, 11 atopic dermatitis, 12 psoriasis, 13 and acne 14 …”