BACKGROUND: Chronic sinusitis is one of the frequent inflammatory diseases and has a complex pathogenesis. A substantial factor seems to be recurrent bacterial infections. Pseudomonas aeruginosa (PA) frequently can be found in nasal smears of patients with persistent sinus symptoms after sinus surgery. Lately a new antimicrobial peptide of epithelial origin, human Beta-Defensin-2 (hBD-2), with a strong antibacterial effect against PA could be identified within lesional skin scales of patients suffering psoriasis. Aim of this study was to investigate hBD-2-mRNA expression in nasal cells and tissue. METHODS: Total RNA was extracted from nasal polyps and turbinates following TRIzol protocol. Epithelial cells and fibroblasts of nasal human tissue were isolated and cultivated. The cells were stimulated with PA using different time points and different concentrations. Total RNA was isolated as mentioned above, reverse transcribed and amplified in a Semi-quantitative Reverse Transcriptase PCR (SQRT-PCR) with genespecific hBD-2 primers. RESULTS: PA induces time- and dose-dependently hBD-2 gene expression in nasal epithelial cells. Unstimulated epithelial nasal cells were able to express hBD-2 mRNA constitutively, whereas nasal fibroblasts showed no hBD-2 mRNA expression. Nasal polyps showed a comparable less hBD-2 gene expression then nasal turbinates. CONCLUSIONS: hBD-2 possibly mediates a specific, early starting antimicrobial defense strategy of the nasal mucosa. This hypothesis would explain persistent infections with PA through diminished hBD-2 gene expression.
BACKGROUND: Chronic sinusitis is one of the frequent inflammatory diseases and has a complex pathogenesis. A substantial factor seems to be recurrent bacterial infections. Pseudomonas aeruginosa (PA) frequently can be found in nasal smears of patients with persistent sinus symptoms after sinus surgery. Lately a new antimicrobial peptide of epithelial origin, humanBeta-Defensin-2 (hBD-2), with a strong antibacterial effect against PA could be identified within lesional skin scales of patients suffering psoriasis. Aim of this study was to investigate hBD-2-mRNA expression in nasal cells and tissue. METHODS: Total RNA was extracted from nasal polyps and turbinates following TRIzol protocol. Epithelial cells and fibroblasts of nasal human tissue were isolated and cultivated. The cells were stimulated with PA using different time points and different concentrations. Total RNA was isolated as mentioned above, reverse transcribed and amplified in a Semi-quantitative Reverse Transcriptase PCR (SQRT-PCR) with genespecific hBD-2 primers. RESULTS: PA induces time- and dose-dependently hBD-2 gene expression in nasal epithelial cells. Unstimulated epithelial nasal cells were able to express hBD-2 mRNA constitutively, whereas nasal fibroblasts showed no hBD-2 mRNA expression. Nasal polyps showed a comparable less hBD-2 gene expression then nasal turbinates. CONCLUSIONS:hBD-2 possibly mediates a specific, early starting antimicrobial defense strategy of the nasal mucosa. This hypothesis would explain persistent infections with PA through diminished hBD-2 gene expression.