BACKGROUND: The formation of nasal polyps is connected with a chronic inflammatory process with the activation of different cytokines. TGF-ss induces fibrosis and acts as a chemoattractant and proliferation factor for fibroblasts. The aim of the study was to evaluate the expression profiles of the genes coding TGF-ss isoforms in nasal polyps with predominately eosinophilic and neutrophilic infiltration and in healthy mucosa and to assess their mutual correlation with the levels of gene transcription. MATERIAL/ METHODS: The study group consisted of 24 patients with nasal polyposis. On the basis of the histopathological evaluation there were 16 eosinophilic and 8 neutrophilic polyps. The control group constituted 9 healthy patients. The expression profiles of the genes coding the TGF-ss isoforms were detected using real-time RT-QPCR. RESULTS: TGF-beta1 and TGF-beta2 mRNAs were revealed in 10 patients with eosinophilic polyps. TGF-beta1 transcriptional activity was accompanied by TGF-beta2 transcriptional activity in nasal polyps. TGF-beta2 gene expression in tissues without mRNA for TGF-beta1 was silenced. There was positive correlation between the expressions of the TGF-beta1 and TGF-beta2 isoforms in nasal polyps. TGF-beta1 mRNA was present at higher levels in all control samples than in eosinophilic polyps. An increased TGF-beta1 mRNA expression was accompanied by an increased TGF-beta2 mRNA expression in healthy mucosa. TGF-beta3 showed the most intensive transcriptional activity among the TGF-ss isoforms in both nasal polyps and control tissues. There was no correlation between TGF-beta3 and TGF-beta1 nor between TGF-beta3 and TGF-beta2 transcriptional activity in nasal polyps and normal tissue.
BACKGROUND: The formation of nasal polyps is connected with a chronic inflammatory process with the activation of different cytokines. TGF-ss induces fibrosis and acts as a chemoattractant and proliferation factor for fibroblasts. The aim of the study was to evaluate the expression profiles of the genes coding TGF-ss isoforms in nasal polyps with predominately eosinophilic and neutrophilic infiltration and in healthy mucosa and to assess their mutual correlation with the levels of gene transcription. MATERIAL/ METHODS: The study group consisted of 24 patients with nasal polyposis. On the basis of the histopathological evaluation there were 16 eosinophilic and 8 neutrophilic polyps. The control group constituted 9 healthy patients. The expression profiles of the genes coding the TGF-ss isoforms were detected using real-time RT-QPCR. RESULTS:TGF-beta1 and TGF-beta2 mRNAs were revealed in 10 patients with eosinophilic polyps. TGF-beta1 transcriptional activity was accompanied by TGF-beta2 transcriptional activity in nasal polyps. TGF-beta2 gene expression in tissues without mRNA for TGF-beta1 was silenced. There was positive correlation between the expressions of the TGF-beta1 and TGF-beta2 isoforms in nasal polyps. TGF-beta1 mRNA was present at higher levels in all control samples than in eosinophilic polyps. An increased TGF-beta1 mRNA expression was accompanied by an increased TGF-beta2 mRNA expression in healthy mucosa. TGF-beta3 showed the most intensive transcriptional activity among the TGF-ss isoforms in both nasal polyps and control tissues. There was no correlation between TGF-beta3 and TGF-beta1 nor between TGF-beta3 and TGF-beta2 transcriptional activity in nasal polyps and normal tissue.