[The profile of expression of transforming growth factor beta1 and TGFbetaRI, TGFbetaRII and TGFbetaRIII genes in nasal polyps]. / Profil ekspresji genów kodujacych TGF-beta1 i jego receptory TGFbetaRI, TGFbetaRII i TGFbetaRIII w polipach nosa.

BACKGROUND: Transforming growth factor beta (TGF-beta) plays an important role in cells proliferation and differentiation as well as in local immunological response. OBJECTIVES: An evaluation of genes expression profile for TGF-beta1 and its receptors TGF-betaRI, TGF-beta RII and TGF-beta betaRIII as well as their potential role in the pathogenesis of nasal polyps in eosynophilic and neutrophilic polyps and in normal nasal mucosa. MATERIAL: Material consisted of 22 patients. Nasal polyps were removed during standard polypectomy or FESS. In the histopathological evaluation there were 16 eosynophilic polyps and 5 neutrophilic ones. The control group consisted of 8 healthy patients from whom healthy nasal mucosa was taken during nasal septoplasty. METHODS: The expression of the genes coding TGF-beta and its receptors was evaluated with the use of RT-PCR technique. RESULTS: TGF-beta1 mRNA was present in 10 eosynophilic polyps out of 16. In neutrophilic polyps group (n = 6) mRNA TGFbeta-1 was present in 3 samples. TGFbeta-1 isoform was present in all the tissues of the control group. It was significantly larger expression of TGFbeta-1 gene in normal mucosa in comparison with eosinophilic and neutrophilic polyps (p < 0.05). The expression of genes coding TGFbetaRI, TGF-betaRII and TGF-betaRIII receptors was obtained in all the polyps and healthy tissues. There was no significant differences in the transcription activity of the receptors in polyps and in the healthy tissue. CONCLUSIONS: Considering regulative function of TGFbeta1 in inflammation processes, its low concentration in nasal polyps tissue may influence on migration and survival of inflammation cells. The high expression of genes coding TGFbetaRI, TGF-betaRII and TGF-betaRIII receptors in all the polyps and healthy tissues, show readiness to transduction of TGFbeta. It may suggest that, less intensive TGFbeta1 expression in nasal polyps may be connected with the presence of other than first TGFbeta isoforms. This problem needs further investigations to set precise role of individual TGFbeta isoforms and other growth factors in the pathogenesis of NSP as their interactions with local cytokines. It may help to work out more effective and specific therapeutic methods in nasal polyps therapy.