International forum of allergy & rhinology · 2025
IL-13-Induced Periostin Expression is Increased in Eosinophilic Chronic Rhinosinusitis.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Suzaki Isao, Hirabayashi Eiko, Teguchi Yuna, Takeuchi Mio, Hirano Kojiro, Shimane Toshikazu, Nunomura Satoshi, Izuhara Kenji, Rubin Bruce K
Аннотация
BACKGROUND: Periostin is an extracellular matrix protein that is highly expressed in nasal polyp (NP) tissues in patients with chronic rhinosinusitis (CRS). This study investigated the cellular source of periostin in sinonasal tissues and the mechanism of IL-13-induced periostin production in nasal epithelial cells.
METHODS: The amount and localization of the periostin protein and mRNA were examined via immunohistochemistry and in situ hybridization analysis in control subjects and subjects with eosinophilic chronic rhinosinusitis (ECRS) and non-ECRS. The expression levels of periostin and type 2 inflammatory cytokines in the tissue were measured by protein and mRNA levels. Normal human nasal epithelial cells were cultured in the presence of IL-13, and the effect of the specific inhibitors, leflunomide, PD98059, or PS1145, on periostin production was evaluated.
RESULTS: Periostin was mainly deposited in the subepithelial region of NP tissues in ECRS and was more highly expressed than in non-ECRS (p < 0.01) and control subjects (p < 0.001). The number of periostin mRNA-positive basal epithelial cells was significantly increased in NP tissues in ECRS. The IL-13 concentration was strongly correlated with periostin expression in the tissues (p < 0.0001, r = 0.8802). Periostin production was much greater in differentiated cells under long-term stimulation with IL-13 than in ciliated cells, and this effect was attenuated by leflunomide and PD98059, but not by PS1145.
CONCLUSION: NP tissues from ECRS patients exhibit increased type 2 inflammatory cytokines and periostin. Nasal epithelial cells, particularly basal cells, are an important source of periostin. Exposure to IL-13 is important for periostin production from nasal epithelial cells.
METHODS: The amount and localization of the periostin protein and mRNA were examined via immunohistochemistry and in situ hybridization analysis in control subjects and subjects with eosinophilic chronic rhinosinusitis (ECRS) and non-ECRS. The expression levels of periostin and type 2 inflammatory cytokines in the tissue were measured by protein and mRNA levels. Normal human nasal epithelial cells were cultured in the presence of IL-13, and the effect of the specific inhibitors, leflunomide, PD98059, or PS1145, on periostin production was evaluated.
RESULTS: Periostin was mainly deposited in the subepithelial region of NP tissues in ECRS and was more highly expressed than in non-ECRS (p < 0.01) and control subjects (p < 0.001). The number of periostin mRNA-positive basal epithelial cells was significantly increased in NP tissues in ECRS. The IL-13 concentration was strongly correlated with periostin expression in the tissues (p < 0.0001, r = 0.8802). Periostin production was much greater in differentiated cells under long-term stimulation with IL-13 than in ciliated cells, and this effect was attenuated by leflunomide and PD98059, but not by PS1145.
CONCLUSION: NP tissues from ECRS patients exhibit increased type 2 inflammatory cytokines and periostin. Nasal epithelial cells, particularly basal cells, are an important source of periostin. Exposure to IL-13 is important for periostin production from nasal epithelial cells.