gms | German Medical Science

78. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie e. V.

Deutsche Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie e. V.

16.05. - 20.05.2007, München

Immunohistochemical proof of Caspase 3 in human nasal mucous mambrane

Meeting Abstract

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German Society of Oto-Rhino-Laryngology, Head and Neck Surgery. 78th Annual Meeting of the German Society of Oto-Rhino-Laryngology, Head and Neck Surgery. Munich, 16.-20.05.2007. Düsseldorf, Köln: German Medical Science; 2007. Doc07hno104

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Veröffentlicht: 8. August 2007

© 2007 Hirt et al.
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The pathogeny of the chronic rhinosinusitis is not until today yet completely known. Inflammatory processes play a central role, at which eosinophil granulocytes take in a decisive role. Through liberated cytokine it comes to inflammatory and remodelling processes. It is unclear to what extent induced apoptosis plays a role to the polyposis nasi, however, in the clinical picture also with other illnesses of the nasal mucous membrane.

Caspase 3 is a key enzyme of the apoptosis cascade which is activated by initiating caspase-enzymes, however, also through cytokines. The comparison of the Caspase 3-activity in probes of nasal mucous tissue of patients with different nasal diseases is objective of the investigation in comparison with a healthy control group.

Of 48 patients in the age of 17-74 years and both sexes, that had to subject themselves to a functional nasal surgery with turbinotomy, tissue probes were taken from the lower turbinate and fixed in 4 % of paraformaldehyde solution. Probes were taken by patients of following illness groups: Polyposis nasi (n=12), Rhinitits allergica (n=7), Rhinitis medicamentosa (n=10) and Rhinitis atrophicans (n=6). 13 healthy patients form the control.

The sections were examined immunhistochemically with polyclonal antibodies against activated Caspase 3 according the ABC-method.

The patients with Polyposis nasi showed a clear reaction in the highly stratified epithelium cells and in the subepithelial sited glands . Furthermore activated Caspase 3 can be proved also in the subepithelial blood vessels. Rhinitis medicamentosa (RM) showed especially in the endothelial cells and the lamina muscularis of the blood vessels a strong activity of Caspase 3. The epithelium and the subepithelial glands at the RM did not show any Caspase 3 activity. The ciliated epithelium and the subepithelial glands at the Rhinitis atrophicans showed a distinctive Caspase 3 activity. In the subepithelial vessels no activated Caspase 3 was detectable. Patients with allergic Rhinitis and in the control group no essential Caspase 3 activity could be found.

Polyposis nasi can enhance the release of cytokines that can activate Caspase 3. Caspase 3 is a key enzyme of the apoptosis cascade and initiates the “programmed cell death”. Apoptosis seems to play an important role next to inflammatory and remodelling processes in the pathogenesis of the chronically hyperplastic rhinosinusitis. The changes of the endothelium at the Rhinitis medicamentosa can be showed by the increasing apoptosis there. Caspase 3-activity in the ciliated epithelium in older patients with Rhinitis atrophicans makes the reduced mucociliary clearance understandable. Apoptosis in the subepithelial glands seems to support atrophic rhinitis.

Further investigations for the induction of Caspase 3 are necessary in order to develop new therapy strategies for the treatment of the different forms of rhinitis.