Human Beta-Defensin-2 in Oral Cancer with Opportunistic Candida Infection

• Published in: Anticancer research 2004-03, Vol.24 (2B), p.1025-1030
• Main Authors: MEYER, Jens Eduard, HARDER, Jürgen, GÖRÖGH, Tibor, WEISE, Jan Bernd, SCHUBERT, Sabine, JANSSEN, Dirk, MAUNE, Steffen
• Format: Article
• Language: English
• Subjects: Base Sequence; beta-Defensins - antagonists & inhibitors; beta-Defensins - biosynthesis; beta-Defensins - genetics; Betamethasone - pharmacology; Biological and medical sciences; Candida albicans; Candidiasis - complications; Candidiasis - genetics; Candidiasis - metabolism; Carcinoma, Squamous Cell - genetics; Carcinoma, Squamous Cell - metabolism; Carcinoma, Squamous Cell - microbiology; Epithelial Cells - metabolism; Epithelial Cells - microbiology; Gene Expression; Humans; Hyperplasia; Medical sciences; Molecular Sequence Data; Opportunistic Infections - complications; Opportunistic Infections - genetics; Opportunistic Infections - metabolism; Opportunistic Infections - microbiology; Otorhinolaryngology. Stomatology; Palatine Tonsil - pathology; RNA, Messenger - biosynthesis; RNA, Messenger - genetics; Tonsillar Neoplasms - genetics; Tonsillar Neoplasms - metabolism; Tonsillar Neoplasms - microbiology; Tumor Cells, Cultured; Tumors; Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology
• ISSN: 0250-7005; 1791-7530

Candida albicans (CA) is a frequent opportunistic pathogen in cancer patients. Usually, human surfaces are protected, apart from physical barriers, by the production of human β-defensins (hBD). hBD-2 shows a potent antimicrobial activity against CA. We therefore investigated whether CA induces hBD-2 expression in primary oral cells and if immunosuppressive betamethasone alters hBD-2 expression. Additionally, we studied, whether a lack of hBD-2 expression could explain opportunistic infection of tonsillar cancer. Primary oral epithelial cells and fibroblasts were stimulated with Candida albicans in a time- and dose-dependent manner with or without betamethasone preincubation. Total RNA from oral cells and specimens was isolated and hBD-2 expression was analyzed by semiquantitative RT-PCR. Our data demonstrate that opportunistic CA induced hBD-2 expression in a time- and dose-dependent manner, suggesting hBD-2 to be a fast antifungal, epithelia-derived immune response. Treatment with glucocorticoid could lead to diminished innate immunity based on suppression of inducible AP. Malignant transformation induces alteration of hBD-2 expression and leads to a reduced hBD-2 expression and subsequentially to Candida colonization on oral SCCs.