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Updated: Aug 9, 2026
Generation and Culturing of Primary Human Keratinocytes from Adult Skin
Published on: December 22, 2017
Cetirizine and hydrocortisone differentially regulate ICAM-1 expression and chemokine release in cultured human
C Albanesi1, S Pastore, E Fanales-Belasio
1Laboratory of Immunology, Istituto Dermopatico dell'Immacolata, IRCCS, Rome, Italy.
Insights
Cetirizine inhibits the activation of skin keratinocytes by blocking immune signaling molecules like ICAM-1. These findings suggest potential benefits for topical cetirizine use in treating skin immune responses.
Area of Science:
- Dermatology
- Immunology
- Pharmacology
Background:
- Cetirizine, a H1 histamine antagonist, has known anti-inflammatory properties.
- Previous research indicates cetirizine inhibits leucocyte recruitment and reduces ICAM-1 expression.
- The anti-inflammatory effects of cetirizine on skin keratinocytes have not been previously studied.
Purpose of the Study:
- To compare the anti-inflammatory effects of cetirizine and hydrocortisone on human keratinocytes activated by IFNgamma.
- To investigate the impact of cetirizine and hydrocortisone on the expression of immune-modulatory molecules and chemokine release from keratinocytes.
Main Methods:
- Human keratinocyte cultures were activated with IFNgamma.
- Cultures were treated with varying concentrations of cetirizine or hydrocortisone.
- Expression of ICAM-1, HLA-DR, MHC class I, CD40, and release of chemokines (RANTES, IL-8, MCP-1, GM-CSF) were measured.
Main Results:
- High concentrations of cetirizine inhibited IFNgamma-induced ICAM-1, HLA-DR, and MHC class I expression, and reduced MCP-1 and RANTES release.
- Hydrocortisone enhanced ICAM-1, reduced HLA-DR, and decreased GM-CSF and IL-8 release.
- Cetirizine's effects on ICAM-1 were confirmed at the mRNA level.
Conclusions:
- Cetirizine effectively blocks IFNgamma-induced keratinocyte activation, suggesting regulatory effects on skin-mediated immune responses.
- The high concentrations needed indicate potential benefits for topical cetirizine application.
- Cetirizine demonstrates anti-inflammatory properties in skin keratinocytes, distinct from hydrocortisone's effects.
Background:
Cetirizine is a H1 histamine antagonist which possesses anti-inflammatory properties through inhibition of leucocyte recruitment and activation, and reduction of ICAM-1 expression on mucosal epithelial cells. No studies have addressed the potential anti-inflammatory activities of cetirizine on skin keratinocytes.
Objectives:
Cetirizine and hydrocortisone were compared in their capacity to counteract human keratinocytes activation by IFNgamma. In particular, expression of immuno-modulatory membrane molecules and chemokine release have been examined.
Methods:
Keratinocyte cultures established from normal skin of healthy donors were activated by IFNgamma (100-500 U/mL) in the absence or presence of cetirizine (10(-3)-10(3) microM) or hydrocortisone (10(-3)-10(2) microM), and tested for expression of ICAM-1, HLA-DR, MHC class I and CD40 as well as for release of RANTES, IL-8, macrophage chemotactic protein-1 (MCP-1) and granulocyte macrophage-colony stimulating factor (GM-CSF).
Results:
Cetirizine at high concentrations (10(2)-10(3) microM) markedly inhibited IFNgamma-induced expression of membrane ICAM-1, HLA-DR and up-regulation of MHC class I, but had no effect on CD40 expression. In contrast, hydrocortisone (10(2) microM) enhanced IFNgamma-induced membrane ICAM-1, reduced expression of HLA-DR and did not alter expression of MHC class I and CD40. Consistently, high doses of cetirizine decreased, whereas hydrocortisone increased, soluble ICAM-1 levels in the supernatants of IFNgamma-treated keratinocytes. The inhibiting and stimulating effects of cetirizine and hydrocortisone, respectively, on ICAM-1 expression were confirmed at the mRNA level by Northern blot analysis. Finally, cetirizine, but not hydrocortisone, inhibited the release of MCP-1 and RANTES from IFNgamma-stimulated keratinocytes. In contrast, hydrocortisone, but not cetirizine, reduced GM-CSF and IL-8 release.
Conclusions:
The results indicate that cetirizine has the capacity to block the IFNgamma-induced activation of keratinocytes, and thus can exert important regulatory effects on TH1 cell-mediated immune responses in the skin. The high doses required for evidencing these activities suggest the potential benefits of a topical use of cetirizine.
