致敏血清誘導大鼠氣道平滑肌細胞嗜酸粒細胞趨化因子的表達及機制探討_《中國呼吸與危重監護雜志》

作者：

高峰 ¹ , 肖鐳 ²

1 徐州醫學院附屬醫院呼吸內科( 江蘇徐州 221002);;
2 鄭州市中心醫院急診科( 河南鄭州 450007) 通訊作者: 肖鐳, E-mail: pponline@ 163. com;

關鍵詞：

Asthma Airway smooth muscle cells Eotaxin Cyclic adenosine monophosphate

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目的觀察氣道平滑肌細胞經哮喘致敏血清刺激后嗜酸粒細胞趨化因子( Eotaxin) 的表達變化, 并探討其可能的機制。方法貼壁法體外培養大鼠氣道平滑肌細胞。建立大鼠哮喘模型,采血收集致敏血清。用致敏血清刺激體外培養的氣道平滑肌細胞, 或同時予以致敏血清和地塞米松干預。采用酶聯免疫吸附法測定培養液上清中Eotaxin 水平, 放射免疫法測定細胞內環磷酸腺苷( cAMP) 表達, 逆轉錄聚合酶鏈反應半定量檢測細胞中Eotaxin mRNA 表達。結果致敏血清干預后,細胞培養上清Eotaxin 水平和細胞內Eotaxin mRNA 表達均較正常對照組顯著升高[ ( 107. 09 ±7. 12) ng/L比( 0. 63 ±0. 56) ng/L, P lt;0. 05; 1. 39 ±0. 04 比0. 05 ±0. 01, P lt;0. 05] , 細胞內cAMP表達顯著降低[ ( 17. 58 ±3. 62) ng/L 比( 32. 39 ±3. 36) ng/L, P lt;0. 05] 。地塞米松與致敏血清同時干預后, 上清中Eotaxin 水平[ ( 64. 18 ±4. 04) ng/L] 和胞內Eotaxin mRNA( 0. 77 ±0. 19) 表達較哮喘組顯著降低, 細胞內cAMP 表達顯著升高[ ( 58. 99 ±5. 94) ng/L] ( P lt; 0. 05) 。上清Eotaxin 水平與胞內cAMP 水平呈負相關( r= - 0. 788, P lt;0. 01) 。結論氣道平滑肌細胞在致敏狀態下Eotaxin 基因和蛋白表達均顯著增強, 可能作為炎性自分泌細胞分泌炎癥因子, 通過cAMP 信號途徑參與哮喘的發生。

引用本文： 高峰,肖鐳. 致敏血清誘導大鼠氣道平滑肌細胞嗜酸粒細胞趨化因子的表達及機制探討. 中國呼吸與危重監護雜志, 2010, 9(5): 490-492. doi: 復制

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11.	張麗娜, 陳萍. 支氣管哮喘靶向治療的新進展. 中國呼吸與危重監護雜志, 2009, 8 : 411-414.
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1. Peng T, Hao L, Madri JA, et al. Role of C5 in the development of airway inflammation, airway hyperresponsiveness, and ongoing airway response. J Clin Invest, 2005 , 115: 1590-1600.
2. Panettieri RA Jr. Airway smooth muscle: immunomodulatory cells that modulate airway remodeling. Respir Physiol Neurobiol, 2003 ,137: 277-293.
3. Xu SY, Xu YJ, Zhang ZX, et al. Contribution of protein kinase C to passively sensitized human airway smooth muscle cells proliferation.Chin Med J( Engl) , 2004, 117: 30 -36.
4. Weltman JK. Cytokines: regulators of eosinophilic inflammation.Allergy Asthma Proc, 2000, 21: 203-207 .
5. Lilly CM, Nakamura H, Kesselman H, et al. Expression of eotaxin by human lung epithelial cells: induction by cytokines and inhibition by glucocorticoids. J Clin Invest, 1997, 99 : 1767 -1773 .
6. Zuyderduyn S, Sukkar MB, Fust A, et al. Treating asthma means treating airway smooth muscle cells. Eur Respir J,2008, 32: 265-274.
7. Tliba O, Panettieri RA Jr. Regulation of Inflammation by airway smooth muscle. Curr Allergy Asthma Rep, 2008, 8: 262-268.
8. Hakonarson H, Grunstein MM. Autocrine regulation of airway smooth muscle responsiveness. Respir Physiol Neurobiol, 2003,137: 263-276.
9. Rahman MS, Yamasaki A, Yang J, et al. I L-17A induces eotaxin-1 /CC chemokine ligand 11 expression in human airway smooth muscle cells: role of MAPK ( Erk1 /2, JNK, and p38) pathways. J Immunol,2006, 177: 4064-4071.
10. Zuyderduyn S, Sukkar MB, Fust A, et al. Treating asthma means treating airway smooth muscle cells. Eur Respir J,2008, 32: 265-274.
11. 張麗娜, 陳萍. 支氣管哮喘靶向治療的新進展. 中國呼吸與危重監護雜志, 2009, 8 : 411-414.
12. Tliba O, Panettieri RA Jr. Noncontractile function of airway smooth muscle cells in asthma. Annu Rev Physiol, 2009, 71: 509 -535.

《中國呼吸與危重監護雜志》

致敏血清誘導大鼠氣道平滑肌細胞嗜酸粒細胞趨化因子的表達及機制探討

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《中國呼吸與危重監護雜志》

致敏血清誘導大鼠氣道平滑肌細胞嗜酸粒細胞趨化因子的表達及機制探討

摘要 全文 圖表 視頻 參考文獻 施引文獻 補充材料

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Content

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