목적: Periostin, a member of the matricellular protein family, is a biomarker of type 2 inflammation in chronic respiratory diseases, including asthma and chronic rhinosinusitis (CRS). Eosinophilic CRS is frequently associated with polyp formation in the nasal mucosa and osteitis in the paranasal sinus bone. However, the role of periostin in tissue remodeling and neo-osteogenesis of patients with CRS remains unclear. Here, we aimed to reveal whether periostin exacerbates or protects the nasal epithelium from tissue remodeling in inflammatory sinonasal diseases. Additionally, we investigated the association between secreted periostin by Th2 inflammation and osteogenesis in eosinophilic CRS (ECRS). 방법:We cultured primary human nasal epithelial cells (HNEC) and fibroblasts (HNF) from nasal polyps. And we examined an in vivo ECRS model in both wild-type (BL6/J) and periostin knockout (KO) mice. 결과:Interleukin-4 increased periostin expression in the cell lysates and media of both nasal respiratory cells. HNFs secreted higher levels of periostin than HNECs, suggesting that HNFs are the main sources of periostin by IL-4 stimulation. We additionally found that secreted periostin from HNFs induced osteoblast differentiation. The wild-type ECRS group showed an increased level of periostin and a thicker epithelium in the nasal mucosa. Furthermore, the periostin KO ECRS group showed less RUNX2 and osteopontin expression than the wild- type ECRS group, indicating that periostin plays a critical role in the neo-osteogenesis during ECRS. 결론:In summary, our results demonstrate that periostin, secreted in response to Th2 cytokine stimulation, reduces polyp formation and mediates osteogenesis in the sinonasal bone during ECRS.