Abstract
Atopic dermatitis (AD) is a recurrent allergic skin disease caused by genetic and environmental factors. Patients with AD may experience immune imbalance, increased levels of mast cells, immunoglobulin (Ig) E and pro-inflammatory factors (Cyclooxygenase, COX-2 and inducible NO synthase, iNOS). While spilanthol (SP) has anti-inflammatory and analgesic activities, its effect on AD remains to be explored. To develop a new means of SP, inflammation-related symptoms of AD were alleviated, and 2,4-dinitrochlorobenzene (DNCB) was used to induce AD-like skin lesions in BALB/c mice. Histopathological analysis was used to examine mast cells and eosinophils infiltration in AD-like skin lesions. The levels of IgE, IgG1 and IgG2a were measured by enzyme-linked immunosorbent assay (ELISA) kits. Western blot was used for analysis of the mitogen-activated protein kinase (MAPK) pathways and COX-2 and iNOS protein expression. Topical SP treatment reduced serum IgE and IgG2a levels and suppressed COX-2 and iNOS expression via blocked mitogen-activated protein kinase (MAPK) pathways in DNCB-induced AD-like lesions. Histopathological examination revealed that SP reduced epidermal thickness and collagen accumulation and inhibited mast cells and eosinophils infiltration into the AD-like lesions skin. These results indicate that SP may protect against AD skin lesions through inhibited MAPK signaling pathways and may diminish the infiltration of inflammatory cells to block allergic inflammation.
Highlights
Common symptoms of atopic dermatitis include itching, redness, and cracking skin
We found that SP exerts its anti-inflammatory activity by suppressing intercellular adhesion molecule 1 (ICAM-1) and COX-2 expression, and blocking the phosphorylated jun N-terminal kinase (JNK) signaling pathway [24]
Our findings indicate that SP reduces Th2-mediated infiltration by mast cells and eosinophils and decreases ear and dorsal skin thickness, and SP inhibits COX-2 and iNOS expression by blocking mitogen-activated protein kinase (MAPK) pathways in mice with DNCB-induced atopic dermatitis (AD)
Summary
Common symptoms of atopic dermatitis ( known as atopic eczema) include itching, redness, and cracking skin. Atopic dermatitis (AD) is the product of a series of complex interactions of innate and adaptive immune responses and IgE-mediated allergies to various exogenous antigens [2]. Studies have found that allergic reactions activate T helper (Th) cells, and that an imbalance between Th1 and Th2 cells causes AD [4]. Mast cells are Th2-activated regulatory cells that release a lot of inflammatory-related cytokines, which can cause inflammation and allergic reaction [7,8]. Th2-activated cells enable the aggregation of eosinophils, causing localized severe inflammation. Decreasing the activity of Th2 cells may improve skin symptoms of AD. Phosphorylation of MAPKs causes the inflammatory mediators’ production and promotes an allergic inflammatory response. Inactivation of MAPKs subsequently decreases the allergic inflammatory response [11,12,13]
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