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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.
Background:
The pathogenesis of melasma remains unclear. Interleukin (IL)-17, a proinflammatory mediator, disturbs barrier function. Filaggrin (FLG) is a protein involved in epidermal barrier homeostasis and may be affected by IL-17 and IL-33.
Objective:
To evaluate epidermal barrier function in malar melasma and its association with the expression of FLG, IL-17, and IL-33.
Methods:
Twenty patients with malar melasma were included in this study. Colorimetric and transepidermal water loss (TEWL) was measured in lesional and adjacent unaffected skin at baseline and 30 minutes after barrier disruption using the tape-stripping test. Biopsies from melasma and perilesional skin were performed to evaluate the presence of FLG by immunohistochemistry, and profilaggrin, IL-17, and IL-33 expression were analyzed by reverse transcription-qualitative polymerase chain reaction.
Results:
After the stripping test, the erythema and TEWL values were higher in the melasma than in the unaffected skin ( P = 0.01). Thirty minutes later, TEWL diminished, but it remained higher than in the perilesional skin. Profilaggrin increased as TEWL gradually decreased (R = -0.68, P = 0.04). FLG and IL-17 were higher in the melasma than in the perilesional skin ( P = 0.003). IL-17 and profilaggrin expression were positively associated (R = 0.60, P = 0.04). IL-33 expression was higher in the adjacent normal skin than in the melasma ( P = 0.01).
Conclusion:
This study found subclinical inflammation in the skin adjacent to the melasma, dysfunction of the epidermal barrier in lesions associated with chronic inflammation, and an abnormal differentiation process promoting an increase in FLG. These findings highlight the need to preserve the integrity of the facial stratum corneum in these patients.
Insights
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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