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題名 | Neutrophil Adherence to Lung Epithelial Cells Induce Interleukin-8 Release=嗜中性白血球黏附於肺部上皮細胞能誘發第八介白質釋放 |
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作者 | 黃建達; 黃國雄; 林鴻銓; 王圳華; 郭漢彬; | 書刊名 | 長庚醫學 |
卷期 | 22:3 1999.09[民88.09] |
頁次 | 頁392-399 |
分類號 | 415.424 |
關鍵詞 | 第八介白質; 嗜中性白血球; 上皮細胞; 黏附分子; Interleukin-8; Neutrophil; Epithelial cell; Adhesion molecule; |
語文 | 英文(English) |
中文摘要 | 背景:嗜中性白血球聚集於肺臟組織並穿透肺上皮細胞進入氣道及肺泡是呼吸道 發炎的明顯特徵。在眾多的發炎前媒介因子,第八介白質對於嗜中性白血球的聚集及黏附扮 演著一個重要的角色。本篇主要去探討嗜中性白血球黏附於肺部上皮細胞對第八介白質分泌 的影響。 方法:在細胞激素(IFNγ+TNFα+IL-1β)的刺激下,定量A549上皮細胞分泌第八介白 質之能力並測量嗜中性白血球黏附於上皮細胞的比例。另在先行以細胞間黏附分子(ICAM-1) 阻斷抗體處理下,評估黏附分子對於調節嗜中性白血球黏附扮演之角色。 結果:上皮細胞第八介白質之分泌呈現時間關連性之增加;嗜中性白血球附著於上皮細 胞的比例也呈現時間關連性之正向變化。當細胞激素(IFNγ+TNFα+IL-1β) 刺激上皮細胞 後,增加第八介白質分泌,同時嗜中性白血球黏附於上皮細胞的比例也隨著增加。加入嗜中 性白血球於上皮細胞會增加第八介白質分泌。先行以細胞間黏附分子(ICAM-1)阻斷抗體處 理上皮細胞後,不論有無細胞激素( IFNγ+TNFα+IL-1β)刺激均抑制嗜中性白血球黏附於上 皮細胞比例,此作用也同時抑制第八介白質分泌。經過膜濾器的處理也明顯降低上皮細胞第 八介白質的分泌。 結論:我們的結果顯示,肺部上皮細胞不僅提供嗜中性白血球活化的處所,也經由其釋 放第八介白質擴大肺部嗜中性白血球的聚集。另外,第八介白質的釋放也與嗜中性白血球黏 附於肺部上皮細胞的比例呈正相關性。 |
英文摘要 | Background: Neutrophil recruitment to the lungs and transmigration through the pulmonary epithelium to reach the respiratory tract are characteristics of airway inflammation. Interleukin-8 (IL-8) plays a critical role in the recruitment of neutrophils to epithelial cells. We investigated the effect of neutrophil adherence to epithelial cells on cytokine secretion. Methods: The production of IL-8 from cultured A549 epithelial cells assayed and neutrophil adherence assay in the presence or absence of interferon-γ(IFN-γ) plus tumor necrosis factor-α (TNF-α) plus interleukin-1β(IL-1β) stimulation was studied on cultured A549 epithelial cells. The role of an adhesion molecule in the modulation of neutrophil adherence was examined by pretreatment with intercellular adhesion molecule-1(ICAM-1) blocking antibody. Results: There was an increase in IL-8 release from epithelial cells that was time-dependent and in the magnitude of neutrophil adherence to the epithelial cells. Stimulation of epithelial cells with IFN-γ +TNF-α+IL-1β significantly increased IL-8 release and neutrophil adherence. The spontaneous of IFN-γ+TNF-α+IL-1β –induced IL-8 release was significantly augmented after the addition of neutrophils. The inhibition of neutrophil adherence to epithelial cells by ICAM-1 blocking antibody downregulated the augmented release of IL-8 with or without IFN-γ+TNF-α +IL-1β stimulation. Placing a membrane filter on cultured cells to prevent neutrophil adherence significantly decreased IL-8 release from epithelial cells with IFN-γ+TNF-α+IL-1β stimulation. Conclusion: Our results indicate that lung epithelial cells not only provide a harboring site for neutrophils to be activated, but also amplify the neutrophil sequestration in the lung by releasing IL-8. Moreover, the release of IL-8 is dependent on the adherence between neutrophils and lung epithelial cells. |
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