Increased in situ expression of melanocortin‐1 receptor in sebaceous glands of lesional skin of patients with acne vulgaris

Abstract

Central or peripheral stress may induce the development of clinical inflammation in the pilosebaceous unit, leading to the development of acne lesions or to exacerbation of pre-existing acne. Melanocortin peptides such as alpha-melanocyte-stimulating hormone and its receptors do not only regulate melanogenesis but can also affect non-pigmentary processes, such as inflammation, apoptosis and sebogenesis. The purpose of the study was to investigate by immunohistochemistry if changes of melanocortin-1 receptor expression exist in acne lesions versus normal skin. In all, 33 patients with acne vulgaris and seven age-matched volunteers without acne participated in the study. Skin biopsies were taken from acne-involved faces, the non-involved thigh skin of the same patients and from normal human skin. Melanocortin-1 receptor immunoreactivity was most prominently detectable in adnexal structures. Sebocytes and keratinocytes of the ductus seboglandularis of acne-involved and non-involved skin showed very intense melanocortin-1 receptor expression in contrast to less intense scattered immunoreactivity in normal skin samples. These data suggest that melanocortin-1 receptor is involved in the pathogenesis of acne.

Beyond acne: Current aspects of sebaceous gland biology and function

“…In addition, CRH significantly induces sebaceous lipids production, IL-6 and -8 synthesis and may up-regulate mRNA levels of 3β-hydroxysteroid dehydrogenase/Δ 5-4 isomerase [102,103]. expression of MC-5R is weaker than that of MC1-R but it has been shown to be a marker of human sebocyte differentiation, since its expression increases in lipid-containing sebocytes [106,107]. As proinflammatory cytokines are up-regulated in acne lesions, sebocytes may respond to these signals with increased MC-1R expression, thereby generating a negative feedback mechanism for α-MSH which exerts direct anti-inflammatory actions, i.e.…”

“…As proinflammatory cytokines are up-regulated in acne lesions, sebocytes may respond to these signals with increased MC-1R expression, thereby generating a negative feedback mechanism for α-MSH which exerts direct anti-inflammatory actions, i.e. inhibition of IL-1-mediated IL-8 secretion [105,106].…”

An update on the role of the sebaceous gland in the pathogenesis of acne

“…63,64 In acne-involved skin, sebocytes and keratinocytes of the ductus seboglandularis showed very intense MC-1R expression in contrast to less intense scattered immunoreactivity in normal skin samples suggesting that this receptor is involved in the initiation of acne. 65 MC-1R expression has been shown to be upregulated by proinflammatory signals. 66,67 As proinflammatory cytokines are upregulated in acne lesions, 68 sebocytes may respond to these signals with increased MC-1R expression, thereby generating a negative feedback mechanism for α-MSH which exerts direct anti-inflammatory actions, i.e., inhibition of IL-1-mediated IL-8 secretion.…”

“…66,67 As proinflammatory cytokines are upregulated in acne lesions, 68 sebocytes may respond to these signals with increased MC-1R expression, thereby generating a negative feedback mechanism for α-MSH which exerts direct anti-inflammatory actions, i.e., inhibition of IL-1-mediated IL-8 secretion. 64,65 Cannabinoid receptors (CR), which mediate the psychopharmacological action of marijuana have been not only localised in the central and peripheral nervous system but also in human skin. CR1 and 2 are expressed in human sebaceous glands, 69 whereas the CB2 and other prototypic endocannabinoids are present in SZ95 sebocytes and may induce in a dose-dependent manner lipid production and cell death.…”

Solodyn and Updates on Topical and Oral Therapies for Acne

“…As mentioned earlier, melanocortins and melanocortin receptors (MC1R-MC5R) have been shown to play a role in sebogenesis [17][18][19]. Moreover, it is known that MC1R is expressed in several cell types of human skin, and MC5R is expressed in human sebaceous glands [17].…”