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Human inflammatory dendritic epidermal cells express a functional histamine H4 receptor
Dorothea Dijkstra1, Holger Stark, Paul L Chazot
1Department of Dermatology and Allergology, Hannover Medical School, Hannover, Germany. dijkstra.dorothea@mh-hannover.de
The Journal of Investigative Dermatology
|February 2, 2008
Summary
Histamine H(4) receptor (H(4)R) is expressed on human inflammatory dendritic epidermal cells (IDECs). Activating H(4)R on IDECs downregulates inflammatory chemokines and cytokines, suggesting therapeutic potential for atopic dermatitis.
Area of Science:
- Immunology
- Dermatology
- Pharmacology
Background:
- Leukocyte histamine H(4) receptor (H(4)R) expression suggests immunomodulatory functions.
- Inflammatory dendritic epidermal cells (IDECs) play a role in skin immunity.
- Understanding H(4)R in IDECs could reveal new therapeutic targets for inflammatory skin conditions.
Purpose of the Study:
- To investigate the expression and function of H(4)R on human IDECs.
- To determine the effect of H(4)R activation on chemokine and cytokine production by IDECs.
- To explore the potential therapeutic implications of H(4)R modulation in inflammatory skin diseases.
Main Methods:
- Investigated H(4)R expression on skin-derived and monocyte-derived IDECs (Mo-IDECs).
- Utilized IFN-gamma to upregulate H(4)R on Mo-IDECs.
- Administered histamine, H(4)R agonists (clobenpropit, 4-methylhistamine), and an H(4)R antagonist (JNJ7777120) to Mo-IDECs.
- Measured production of Th2-linked chemokine CCL2 and Th1 cytokine IL-12.
- Assessed monocyte migration in response to CCL2 downregulation.
Main Results:
- H(4)R is expressed on IDECs and its expression is upregulated by IFN-gamma on Mo-IDECs.
- Histamine and H(4)R agonists significantly downregulated CCL2 and IL-12 production by Mo-IDECs.
- An H(4)R-selective antagonist blocked these effects, confirming H(4)R specificity.
- CCL2 downregulation by H(4)R activation led to reduced monocyte migration.
Conclusions:
- Human IDECs express a functionally active H(4)R.
- H(4)R stimulation on IDECs downregulates key inflammatory mediators (CCL2, IL-12).
- H(4)R agonists may offer a therapeutic strategy for inflammatory skin conditions like atopic dermatitis by reducing inflammation and monocyte recruitment.
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