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Stress response, tachykinin, and cutaneous inflammation
I Katayama1, S J Bae, Y Hamasaki
1Department of Dermatology, Nagasaki University School of Medicine, Sakamoto, Japan.
The Journal of Investigative Dermatology. Symposium Proceedings
|January 5, 2002
Summary
Glucocorticoids (GCs) can worsen skin inflammation and itching, contrary to their anti-inflammatory reputation. Unsuitable topical GC use, alongside stress, may disrupt skin immune function via abnormal substance P and cytokine production.
Area of Science:
- Immunology
- Dermatology
- Pharmacology
Background:
- Glucocorticoid (GC) actions on immune cells are increasingly recognized.
- Clinical observations link stress to exacerbated dermatologic diseases.
Purpose of the Study:
- To investigate if GCs modulate cutaneous inflammatory reactions beyond their known anti-inflammatory effects.
- To clarify the impact of topical GC application on skin immune responses.
Main Methods:
- Murine models were used to study contact sensitivity, irritant reactions, and IgE-mediated reactions.
- Effects of topical GC application, high-dose steroids, and withdrawal on scratching behavior were assessed.
- In vitro experiments examined GC effects on cytokine and substance P production in keratinocytes.
Main Results:
- Topical GCs significantly augmented various inflammatory skin reactions in mice.
- Steroid withdrawal enhanced scratching behavior, correlating with preprotachykinin mRNA expression.
- Low-dose GCs upregulated IL1alpha production and induced substance P in keratinocytes.
Conclusions:
- Unsuitable topical GC use and stress-induced GCs may impair skin immune function.
- Aberrant production of tachykinins like substance P and epidermal cytokines are implicated.
- GCs may have pro-inflammatory roles in specific skin contexts.