Cytokine Production from Cultured Nasal Mucosal Epithelium by Staphylococcus Aureus Enterotoxin Stimulation—Comparison with Mite Antigen Stimulation—

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  • 黄色ブドウ球菌エンテロトキシン刺激による培養鼻粘膜上皮からのサイトカイン産生
  • 黄色ブドウ球菌エンテロトキシン刺激による培養鼻粘膜上皮からのサイトカイン産生 : ダニ抗原刺激との比較
  • オウショクブドウキュウキン エンテロトキシン シゲキ ニ ヨル バイヨウ ビ ネンマク ジョウヒ カラ ノ サイトカイン サンセイ : ダニ コウゲン シゲキ ト ノ ヒカク
  • ―ダニ抗原刺激との比較―

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<p>Infection and inflammation enhance hyper-sensitivity of the airway mucosa, and promote the onset and severity of allergic diseases. In this study, commercial non-inflammatory cultured nasal epithelial cells were set up to elucidate the inflammatory reaction based on analyzing cytokine production by stimulation of S. aureus enterotoxin and/or house dust mite antigen directly on the nasal epithelium without effects from the network of infiltrating leukocytes or subepithelial matrix. </p><p>A culture experiment using human nasal epithelial cells was performed. Single or co-stimulation was carried out with S. aureus enterotoxin B (0, 5, 10 μg/ml) and mite antigen (Der f 1) (0, 5, 10 μg/ml), and cytokines in the culture supernatant were quantified by ELISA. Although IL-4, 13, 17, 25, 33, and TNF-α were not detected, IL-5 and 8 were detected after the stimulation with Der f 1 and enterotoxin B. However, dose dependency between the stimulation and cytokine products was not observed. IL-6 production tended to increase in a dose-dependent manner 24 hours after stimulation with Der f1 and enterotoxin B. Synergistic effects from the two types of stimulation were not observed. Although VEGF production tended to increase in a dose-dependent manner after stimulation with Der f1, it conversely decreased by stimulation with a higher dose of enterotoxin B within 24 hours. After stimulation with 5 or 10 μg/ml of enterotoxin B, VEGF production tended to increase in a dose-dependent manner. </p><p>It has been reported that some cytokines affect other cytokine production in epithelial cells. Taking this into account, IL-6 and VEGF production may indirectly affect other cytokines, as well as each other, via cytokine receptors on epithelial cells. </p>

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