We all know the pathophysiological factors required for the development of acne; however, new research suggests the skin cells outside of these hair follicles play a larger role.

You might not believe how. Cells outside the hair follicle are at play – the fibroblasts and their secretion of an antimicrobial peptide called cathelicidin (Camp), in response to acne-causing Cutibacterium acnes.


The study was triggered by knowledge of fibroblasts that become antimicrobial when triggered by TLR2 (a pattern recognition receptor known to influence the inflammatory response) to differentiate into adipocytes as an innate immune defence, particularly against Staphylococcus aureus.

Without the details, analysis of inflamed skin of acne patients after retinoid treatment also showed enhanced induction of cathelicidin, a previously unknown beneficial effect of retinoids in difficult-to-treat
acne.

While the study did show that dermal fibroblasts are involved in acne, the factors that trigger their stimulation and differentiation are relatively unknown. Overall, these data provide evidence that adipogenic fibroblasts are a critical component of the pathogenesis of acne and represent a
potential target for therapy.

Retinoids are effective therapeutics in the treatment of acne. Their mechanism of action has been attributed to suppressive activity on the sebaceous gland or keratinocytes. Isotretinoin down-regulates TLR2 signalling in monocytes and reduces overall inflammation in acne – this appears to be in effect with topical retinoids.