Conflicts of interest None declared.
Intercellular adhesion molecule-1: a consistent inflammatory marker of the cutaneous radiation reaction both in vitro and in vivo
Article first published online: 28 JUN 2006
British Journal of Dermatology
Volume 155, Issue 4, pages 670–679, October 2006
How to Cite
Müller, K., Köhn, F.-M., Port, M., Abend, M., Molls, M., Ring, J. and Meineke, V. (2006), Intercellular adhesion molecule-1: a consistent inflammatory marker of the cutaneous radiation reaction both in vitro and in vivo. British Journal of Dermatology, 155: 670–679. doi: 10.1111/j.1365-2133.2006.07407.x
- Issue published online: 28 JUN 2006
- Article first published online: 28 JUN 2006
- Accepted for publication 25 February 2006
- cutaneous radiation reaction;
- intercellular adhesion molecule-1;
- ionizing radiation;
- three-dimensional skin organ model
Background Radiation damage to skin is a key diagnostic and prognostic parameter for patients accidentally exposed to radiation. Moreover, skin is a target organ for crucial side-effects of routine radiotherapy. The pathophysiology of the cutaneous radiation reaction is in many respects still unknown. The acute inflammatory radiation reaction of skin has been shown to involve alterations in cell–cell and cell–matrix interactions, which are mediated by cellular adhesion molecules.
Objectives To evaluate the effect of ionizing radiation on intercellular adhesion molecule-1 (ICAM-1) expression in human skin cells.
Methods Dermal monolayer cells, a three-dimensional skin model and skin biopsies were investigated for ICAM-1 expression after ionizing radiation using flow cytometry, quantitative reverse transcription–polymerase chain reaction and immunohistochemistry. ICAM-1 expression in monolayer cells pretreated with protein kinase inhibitors and dexamethasone prior to irradiation was analysed by flow cytometry.
Results Using different sources of skin cells, we demonstrated a consistent upregulation of both ICAM-1 mRNA and protein expression by ionizing radiation. Blocking experiments revealed that tumour necrosis factor-α, another ICAM-1 inducer, does not account for the effect of radiation. Radiation-induced upregulation of ICAM-1 expression was significantly attenuated by inhibitors to protein kinase C, mitogen-activated protein (MAP) ERK kinase, p38 MAP kinase and phosphatidylinositol 3-kinase. The anti-inflammatory agent dexamethasone suppressed the effect of radiation on ICAM-1 expression, suggesting its usefulness to treat the cutaneous radiation reaction.
Conclusions Our data suggest that ICAM-1 is a consistent inflammatory parameter of the cutaneous radiation reaction both in vitro and in vivo that might provide new therapeutic options for diagnosis and treatment of effects of radiation.