| セッション情報 |
ポスター
食道 他
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| タイトル |
P-038：Basolaterally expressed PAR-2 in esophageal stratified epithelial cell layers is involved in trypsin-induced impaired epithelial barrier function and IL-8 secretion
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| 演者 |
単 晶（兵庫医科大学内科学上部消化管科） |
| 共同演者 |
大島 忠之（兵庫医科大学内科学上部消化管科）, 神谷 紀子（兵庫医科大学内科学上部消化管科）, 戸川 昌代（兵庫医科大学内科学上部消化管科）, 富田 寿彦（兵庫医科大学内科学上部消化管科）, 福井 広一（兵庫医科大学内科学上部消化管科）, 渡 二郎（兵庫医科大学内科学上部消化管科）, 三輪 洋人（兵庫医科大学内科学上部消化管科） |
| 抄録 |
Immune-mediated injury by the protease-activated receptor-2-interleukin-8（PAR-2-IL8）pathway may underlie the development of gastroesophageal reflux disease（GERD）. However, the localization of PAR-2 and the mechanism of PAR-2 activation remain unclear. This study aimed to address these questions on an esophageal stratified squamous epithelial model and in the human esophageal mucosa of GERD patients. Normal human esophageal epithelial cells（HEEC）were cultured with the air-liquid interface（ALI）system to establish the model. SLIGKV-NH2（a PAR-2 synthetic agonist）, trypsin（a PAR-2 natural activator）and weak acid were added to either the apical or basolateral compartment to evaluate their effects on trans-epithelial electrical resistance（TEER）and IL-8 production. PAR-2 localization was examined by immunohistochemistry. Apical trypsin stimulation induced IL-8 accompanied by decreased TEER in vitro, while the effective concentration from the basolateral side was 10 times lower. SLIGKV-NH2 from basolateral but not apical stimulation induced IL-8 production. Apical weak acid stimulation did not influence TEER or IL-8 production. Immunohistochemistry showed intense reactivity of PAR-2 in the basal and suprabasal layers after stimulation with trypsin and in GERD patients. In conclusion, the activation of the PAR-2-IL-8 pathway probably occurred at the basal and suprabasal layers, while the esophageal epithelial barrier may influence the activation of PAR-2. |
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