gms | German Medical Science

Introduction: The knowledge about the etiology of chronic sinusitis with nasal polyps (CRSwNP) grows also by analog circuits to the immunological principles of other proliferative and inflammatory diseases. The formation of polyps is ultimately based on a disturbance of cell cycle control. STAT3 is a phosphokinase and a key molecule for the regulation of many cellular functions including cell growth.

Methods: We investigated in tissue specimens of polyps, nasal turbinates of patients with CRSwNP and nasal turbinates of patients with healthy mucosa the amount of RNA using DNA microarray, the expression of the protein STAT3 protein by Western blot, the amount of the phosphorylated and thus active form pSTAT3 by protein array and Western blot and the distribution of STAT3 and pSTAT3 in the tissue by immunohistochemistry.

Results: We found no differences regarding the concentration of mRNA and the expression level of the non-phosphorylated protein between the 3 groups. The amount of pSTAT3 was elevated in the tissues of polyps compared with both control groups (p <0.01). There was a clear difference in the distribution of pSTAT3 in the tissue. We found pSTAT3 especially in the superficial layer of the epithelium of the nasal turbinates, but not in the basal layer. In the tissue of the nasal polyps pSTAT3 was localized in all epithelial layers, but significantly increased in the basal cells.

Conclusion: Our data show a different localization and activation of STAT3 in the tissue of the nasal polyps. The results suggest a key role of STAT3 in the development of CRSwNP.