Abstract
The critical roles of keratinocytes and resident mast cells in skin allergy and inflammation have been highlighted in many studies. Cyclic adenosine monophosphate (cAMP), the intracellular second messenger, has also recently emerged as a target molecule in the immune reaction underlying inflammatory skin conditions. Here, we investigated whether undecane, a naturally occurring plant compound, has anti-allergic and anti-inflammatory activities on sensitized rat basophilic leukemia (RBL-2H3) mast cells and HaCaT keratinocytes and we further explored the potential involvement of the cAMP as a molecular target for undecane. We confirmed that undecane increased intracellular cAMP levels in mast cells and keratinocytes. In sensitized mast cells, undecane inhibited degranulation and the secretion of histamine and tumor necrosis factor α (TNF-α). In addition, in sensitized keratinocytes, undecane reversed the increased levels of p38 phosphorylation, nuclear factor kappaB (NF-κB) transcriptional activity and target cytokine/chemokine genes, including thymus and activation-regulated chemokine (TARC), macrophage-derived chemokine (MDC) and interleukin-8 (IL-8). These results suggest that undecane may be useful for the prevention or treatment of skin inflammatory disorders, such as atopic dermatitis, and other allergic diseases.
Highlights
Mast cells are hematopoietic cells derived in the bone marrow from progenitor cells
We found that undecane had no effect on the cell viability of HaCaT cells at all concentrations except 100 μM compared to the control group (Figure 1C)
We further measured Cyclic adenosine monophosphate (cAMP) concentration to examine whether the inhibitory effect of undecane on cell degranulation was related to intracellular cAMP
Summary
Mast cells are hematopoietic cells derived in the bone marrow from progenitor cells. They are involved in the pathophysiology of allergic diseases, especially in IgE-mediated hypersensitivity reactions in the skin and gastrointestinal tract, such as atopic dermatitis (AD) and asthma [1,2].Mast cells express the high-affinity IgE receptor, FcεRI, on their surface and can be stimulated by antigen-regulated aggregation of IgE bound to the receptor. Mast cells are hematopoietic cells derived in the bone marrow from progenitor cells. They are involved in the pathophysiology of allergic diseases, especially in IgE-mediated hypersensitivity reactions in the skin and gastrointestinal tract, such as atopic dermatitis (AD) and asthma [1,2]. Antigen leads to degranulation of mast cells, secreting a broad array of mediators, such as cytokines/chemokines and biogenic amines including tumor necrosis factor α (TNF-α) and histamine [3,4]. Activated keratinocytes release a variety of proinflammatory cytokines and chemokines that can sustain allergic reactions, possibly contributing to AD [6]
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