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Published on: January 19, 2024
Skin Barrier Function and Its Relationship With IL-17, IL-33, and Filaggrin in Malar Melasma
Juan Pablo Castanedo-Cázares1, Juan Diego Cortés-García, Gabriela Pérez-Coronado
1Dermatology Department, Hospital Central Dr. Ignacio Morones Prieto, Facultad de Medicna, Universidad Autónoma de San Luis Potosí, San Luis Potosí, México.
Melasma involves skin barrier dysfunction and inflammation, with increased filaggrin (FLG) and interleukin-17 (IL-17) in lesions. Protecting the facial stratum corneum is crucial for managing melasma.
Area of Science:
- Dermatology
- Skin Biology
- Immunology
Background:
- Melasma pathogenesis is unclear, but inflammation and barrier disruption are implicated.
- Interleukin-17 (IL-17) is a proinflammatory mediator affecting barrier function.
- Filaggrin (FLG) is vital for epidermal barrier homeostasis and may be influenced by IL-17 and IL-33.
Purpose of the Study:
- Evaluate epidermal barrier function in malar melasma.
- Assess the association between melasma and the expression of FLG, IL-17, and IL-33.
Main Methods:
- Assessed barrier function using colorimetry and transepidermal water loss (TEWL) via tape stripping in 20 melasma patients.
- Analyzed FLG, profilaggrin, IL-17, and IL-33 expression in melasma and perilesional skin biopsies using immunohistochemistry and RT-qPCR.
Main Results:
- Melasma skin showed higher erythema and TEWL post-stripping compared to unaffected skin.
- FLG and IL-17 expression were elevated in melasma lesions, positively correlating with each other.
- IL-33 expression was higher in adjacent normal skin than in melasma lesions.
Conclusions:
- Melasma exhibits subclinical inflammation adjacent to lesions and epidermal barrier dysfunction.
- Chronic inflammation in melasma is linked to impaired barrier function and abnormal FLG differentiation.
- Maintaining facial stratum corneum integrity is essential for melasma management.
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