Elisabeth Schremmer-Danninger, 1. Department of Clinical Chemistry and Clinical Biochemistry, Hospital of Surgery, Ludwig-Maximilians-University Munich, Nussbaumstrasse 20, D-80336 Munich, Germany and Department of Clinical and Experimental Pharmacology, Nelson R. Mandela School of Medicine, University of Natal, Private Bag 7, Congella, Durban 4013, South Africa
1 Strinivasen Naidoo, 2. Department of Clinical and Experimental Pharmacology, Nelson R. Mandela School of Medicine, University of Natal, Private Bag 7, Congella, Durban 4013, South Africa
2 Christiane Neuhof, 3. Department of Pathophysiology and Experimental Medicine, Justus-Liebig-University Giessen, Klinikstrasse 36, D-35392 Giessen, Germany
3 Klaus Valeske, 4. Department of Pathophysiology and Experimental Medicine, Justus-Liebig-University Giessen, Klinikstrasse 36, D-35392 Giessen, Germany
4 Celia Snyman, 5. Department of Clinical and Experimental Pharmacology, Nelson R. Mandela School of Medicine, University of Natal, Private Bag 7, Congella, Durban 4013, South Africa
5 Christian Sander, 6. Hospital of Dermatology, Ludwig-Maximilians-University Munich, Frauenlobstrasse 9-11, D-80337 Munich, Germany
6 Kanti D. Bhoola, 7. Department of Clinical and Experimental Pharmacology, Nelson R. Mandela School of Medicine, University of Natal, Private Bag 7, Congella, Durban 4013, South Africa; Asthma and Allergy Research Institute, The University of Australia, Sir Charles Gairdner Hospital, Hospital Avenue, Nedlands WA 6009, Australia
7 Heinz Neuhof8. Department of Pathophysiology and Experimental Medicine, Justus-Liebig-University Giessen, Klinikstrasse 36, D-35392 Giessen, Germany
8 Citation Information. Biological Chemistry. Volume 385, Issue 11, Pages 1069–1076, ISSN (Print) 1431-6730, DOI: 10.1515/BC.2004.138, November 2004
Publication History: Received: //; accepted: //; published online: 01/06/2005
Abstract
During dermal injury and inflammation the serine proteases kallikreins cleave endogenous, multifunctional substrates (kininogens) to form bradykinin and kallidin. The actions of kinins are mediated by preferential binding to constitutively expressed kinin-B2 receptors or inducible kinin-B1 receptors. A feature of the kinin-B1 receptors is that they show low levels of expression, but are distinctly upregulated following tissue injury and inflammation. Because recent evidence suggested that kinin-B1 receptors may perform a protective role during inflammation, we investigated the specific occurrence of the kallikrein-kinin components in skin biopsies obtained from normal skin, patients undergoing surgery, basalioma, lichenificated atopic eczema, and psoriasis. The tissue was immunolabelled in order to determine the localisation of tissue pro-kallikrein, kallikrein, kininogen and kinin receptors. The kinin components were visualised in normal, diseased and traumatised skin, except that no labelling was observed for kininogen in normal skin. Of the five types of tissue examined, upregulation of kinin-B1 receptors was observed only in skin biopsies obtained following surgery. In essence, the expression of kinin-B1 receptors did not appear to be enhanced in the other biopsies. Within the multiple steps of the inflammatory cascade in wound healing, our results suggest an important regulatory role for kinin-B1 receptors during the first phase of inflammation following injury.
Keywords basalioma (basal cell carcinoma), inflammation, kinin-B1 receptor upregulation, lichenificated atopic eczema, psoriasis
