Methods: We investigated periostin expression and its cellular origins in uncinate process mucosa (UP) and nasal polyp (NP) tissues by immunohistochemistry (IHC), quantitative reverse transcription PCR (qRT-PCR), and enzyme-linked immunosorbent assay (ELISA). Correlations between periostin expression and other inflammatory markers, including of interleukin (IL)-5, IL-13, IL-17A, interferon (IFN)-γ, were also explored.
Results: Periostin expression was upregulated in NP mucosa from patients with CRSwNP compared with the uncinate process (UP) tissue of control, CRSsNP and CRSwNP patients. Overexpression of periostin in eosinophilic NP compared to non-eosinophilic NP was confirmed by qRT-PCR, and ELISA. There was a positive correlation between periostin protein concentration and Lund-Mackay CT scores in eosinophilic NP.
Double IHC staining showed that tryptase+ cells were one of the main sources of periostin among immune cells. In addition, periostin mRNA expression was positively correlated with the expression of tryptase+ cells and total IgE homogenate in eosinophilic NP. Overexpression of epithelial integrin αV was detected in NP mucosa from CRSwNP patients compared with UP from control and CRSsNP. Moreover, in eosinophilic NP, the expression of epithelial integrin αV was higher than non-eosinophilic NP and positively correlated with the concentration of periostin. Furthermore, periostin mRNA expression in eosinophilic NP patients was positively correlated with IL-5, IL-13 and negatively related with IL-17A; however, there was no association between those and IFN-γ.
Conclusions: Our data suggest a role for periostin in the pathogenesis of nasal polypogenesis, especially in eosinophilic NP. Therefore, periostin protein might be a new treatment target for patients with CRSwNP.