Human sebum extract induces barrier disruption and cytokine expression in murine epidermis. Issue 1 (April 2015)

• Record Type: Journal Article
• Authors: Guo, Jiun-Wen; Lin, Tzu-Kai; Wu, Chin-Han; Wei, Kai-Che; Lan, Cheng-Che E.; Peng, Amy Chia-Ying; Tsai, Jui-Chen; Sheu, Hamm-Ming
• Is Part Of: Journal of dermatological science. Volume 78:Issue 1(2015:Apr.)
• Page Start: 34
• Page End: 43
• Publication Date: 2015-04
• Subjects: Human sebum -- Epidermal barrier function -- Cytokine expression -- Morphology -- Dermatitis; Dermatology -- Periodicals; Skin Diseases -- Periodicals; Dermatologie -- Périodiques; 616.5005
• DOI: 10.1016/j.jdermsci.2015.01.010
• Languages: English
• ISSNs: 0923-1811

Abstract

Highlights: Sebum imparts detrimental effects on skin permeability barrier of hairless mice. Skin barrier disruption by sebum elicits an epidermal inflammatory cascade. Sebum-induced dermatitis resembles irritant contact dermatitis. Abstract: Background: Previous studies have shown that human sebum may play a role in barrier function but with much debate. Objective: To elucidate the effects of human sebum on skin barrier function. Methods: We used hairless mouse skin to study the functional and morphological alternation of epidermis after the application of human sebum. Results: The results showed a significant increase in transepidermal water loss and erythema value, and a decrease in skin hydration, accompanied by epidermal hyperplasia with parakeratosis following sebum application. Nile red staining together with electron microscopic examination confirmed the underlying mechanisms for sebum-induced barrier disruption are related directly to the interaction of sebum with the intracellular lipid lamellae of the SC, thereby leading to the increase in the fluidity of SC intracellular lipids as demonstrated by ATR-FTIR measurement. An inflammatory reaction characterized by an enhanced cytokine cascade, including up-regulation of TNF-α, IL-1α and IL-6, was also observed. On the other hand, there were insignificant expression of thymic stromal lymphopoietin and unchanged serum levels of IgE, suggesting non-immunogenic stimulation by sebum treatment. Conclusion: It may be concluded that inflammation induced by excess amount of sebum is more likely an irritant contact dermatitis rather than an allergic one. Moreover, these findings implicated possible relationships between sebum, irritant contact dermatitis, and seborrheic dermatitis.