Relationship between transient receptor potential vanilloid-1 expression and the intensity of sensitive skin symptoms.

BACKGROUND: Sensitive skin (SS) is a hyper-reactive condition of the skin secondary to external factors, without objective signs of lesion. Its pathogenesis is still under investigation. Transient receptor potential vanilloid-1 (TRPV1) is a cation channel that responds to low pH and is related to nociception, neurogenic inflammation, and pruritus. AIMS: To determine the expression of TRPV1 in subjects with SS and correlate it with the degree of symptoms and skin pigmentation. PATIENTS/METHODS: We included 31 subjects self-diagnosed as having SS. Colorimetric values were obtained for assessment of skin phototype, and the lactic acid stinging test (LAST) was performed. Two skin biopsies from the nasolabial fold of each volunteer were obtained. Qualitative analysis of TRPV1 was carried out with immunohistochemistry. Quantitative analysis of TRPV1 was carried out with qRT-PCR. RESULTS: LAST was positive in 74% of the subjects, 56% of those having tan and brown skin. Immunohistochemistry staining for TRPV1 was greater in positive subjects (P = 0.03), but showed no correlation with the intensity of symptoms. Positive subjects also had higher TRPV1 mRNA expression compared to negative subjects (P < 0.001). This expression showed a positive correlation with the intensity of referred symptoms (R = 0.75, P < 0.001) and skin pigmentation (R = 0.63, P < 0.001). CONCLUSIONS: TRPV1 expression is upregulated in subjects with sensitive skin, and it correlates with the intensity of the symptoms. Our findings suggest a role for this receptor in the pathogenesis of sensitive skin syndrome.

CD4, IL-17, and COX-2 Are Associated With Subclinical Inflammation in Malar Melasma.

The pathogenesis of melasma, a common, photo-induced hyperpigmentary disorder, is not clearly understood. Significant factors linked to melasma are ultraviolet radiation exposure and genetic predisposition. Histological analysis has demonstrated that melasma is caused by a network of cellular interactions among melanocytes, keratinocytes, mast cells, fibroblasts, and dermal vasculature exhibits, features similar to chronic sun damage. Dermal inflammation caused by ultraviolet radiation might play an important role in the hyperpigmentation and reactivation of melasma lesions through the production of melanogenic cytokines and growth factors. Because the role of inflammation in this disorder is unknown, we used histochemistry, immunohistochemistry, and quantitative real-time polymerase chain reaction to evaluate melasma lesions from healthy female patients (n = 20) with malar melasma. Lesional skin without specific solar exposure or photoprotection measures within the previous 4 weeks was compared with nonlesional skin. The increased lymphocytic infiltrate in lesional skin was mainly composed of CD4 T cells, mast cells, and macrophages. Levels of the cytokine interleukin (IL)-17 and the proinflammatory mediator cyclooxygenase (COX)-2 were significantly elevated in affected skin compared with healthy skin. In addition, the Melasma Activity and Severity Index score, fraction of solar elastosis, and epidermal melanin were positively associated with COX-2 expression. There was no statistically significant difference in IL-1α, IL-1ß, R-IL1, IL-6, IL-8, vascular endothelial growth factor, and tumor necrosis factor alpha expression levels. Together, these data indicated that melasma under unchallenged conditions is characterized by chronic inflammatory cells and mediators, which may explain its recurrent nature.