Effect of a topical steroid on gene expressions for chemokines in mice with contact hypersensitivity
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Updated: Aug 26, 2026
Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis
Published on: September 26, 2022
Gaku Mitsui1, Takeo Hirano, Yoshimi Niwano
1Department of Human Gene Research, Kazusa DNA Research Institute, 2-6-7 Kazusa-kamatari, Kisarazu, Chiba 292-0818, Japan.
Abstract:
Effects of a topical corticosteroid drug, diflucortolone valerate, on the mRNA expressions for four CC- and four CXC-chemokines, which have been reported to be associated with recruitment of different kinds of proinflammatory and inflammatory cells, were investigated by RT-PCR in mice with 2,4,6-trinitrochlorobenzene (TNCB)-induced contact hypersensitivity (CHS) response. All of the eight gene expressions were clearly up-regulated in the lesion site of the CHS response up to 24 h post-challenge of TNCB at which ear swelling response reached a peak, so that heavy infiltration of inflammatory cells consisting mainly of mononuclear cells and neutrophils was likely induced by these chemokines. Topical treatment with diflucortolone valerate suppressed completely the infiltrates as well as the ear swelling response. In addition, the up-regulation of gene expressions for these eight chemokines were suppressed by the treatment, indicating that the corticosteroid drug attenuates the expression of chemokine genes essential for orientating nonspecific skin response to hapten-specific CHS response through the recruitment of inflammatory cells from the circulation into the tissue site.
Insights
Diflucortolone valerate, a topical corticosteroid, effectively reduced skin swelling and inflammatory cell infiltration in mice. The drug also suppressed the expression of key chemokine genes involved in the contact hypersensitivity response.
Area of Science:
- Immunology
- Dermatology
- Pharmacology
Background:
- Contact hypersensitivity (CHS) involves inflammatory cell recruitment mediated by chemokines.
- Chemokines play a crucial role in orchestrating the inflammatory response in skin conditions.
Purpose of the Study:
- To investigate the effects of diflucortolone valerate on chemokine mRNA expression in a mouse model of TNCB-induced CHS.
- To determine if diflucortolone valerate modulates the expression of CC- and CXC-chemokines associated with inflammatory cell infiltration.
Main Methods:
- Contact hypersensitivity was induced in mice using 2,4,6-trinitrochlorobenzene (TNCB).
- Reverse transcription polymerase chain reaction (RT-PCR) was used to quantify mRNA expression of eight chemokines (four CC and four CXC).
- Mice were treated topically with diflucortolone valerate, and ear swelling and inflammatory cell infiltration were assessed.
Main Results:
- TNCB challenge led to significant up-regulation of eight chemokine genes at the lesion site.
- This up-regulation correlated with peak ear swelling and substantial infiltration of mononuclear cells and neutrophils.
- Topical diflucortolone valerate completely suppressed ear swelling, inflammatory infiltrates, and the up-regulation of chemokine gene expression.
Conclusions:
- Diflucortolone valerate effectively attenuates the contact hypersensitivity response in mice.
- The anti-inflammatory effects of diflucortolone valerate are mediated, in part, by suppressing chemokine gene expression.
- This suppression inhibits the recruitment of inflammatory cells, thereby reducing skin inflammation.
