目的 觀察氣道平滑肌細(xì)胞經(jīng)哮喘致敏血清刺激后嗜酸粒細(xì)胞趨化因子( Eotaxin) 的表達(dá)變化, 并探討其可能的機(jī)制。方法 貼壁法體外培養(yǎng)大鼠氣道平滑肌細(xì)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(yǎng)的氣道平滑肌細(xì)胞, 或同時(shí)予以致敏血清和地塞米松干預(yù)。采用酶聯(lián)免疫吸附法測(cè)定培養(yǎng)液上清中Eotaxin 水平, 放射免疫法測(cè)定細(xì)胞內(nèi)環(huán)磷酸腺苷( cAMP) 表達(dá), 逆轉(zhuǎn)錄聚合酶鏈反應(yīng)半定量檢測(cè)細(xì)胞中Eotaxin mRNA 表達(dá)。結(jié)果 致敏血清干預(yù)后,細(xì)胞培養(yǎng)上清Eotaxin 水平和細(xì)胞內(nèi)Eotaxin mRNA 表達(dá)均較正常對(duì)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(xì)胞內(nèi)cAMP表達(dá)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(shí)干預(yù)后, 上清中Eotaxin 水平[ ( 64. 18 ±4. 04) ng/L] 和胞內(nèi)Eotaxin mRNA( 0. 77 ±0. 19) 表達(dá)較哮喘組顯著降低, 細(xì)胞內(nèi)cAMP 表達(dá)顯著升高[ ( 58. 99 ±5. 94) ng/L] ( P lt; 0. 05) 。上清Eotaxin 水平與胞內(nèi)cAMP 水平呈負(fù)相關(guān)( r= - 0. 788, P lt;0. 01) 。結(jié)論 氣道平滑肌細(xì)胞在致敏狀態(tài)下Eotaxin 基因和蛋白表達(dá)均顯著增強(qiáng), 可能作為炎性自分泌細(xì)胞分泌炎癥因子, 通過(guò)cAMP 信號(hào)途徑參與哮喘的發(fā)生。
引用本文： 高峰,肖鐳. 致敏血清誘導(dǎo)大鼠氣道平滑肌細(xì)胞嗜酸粒細(xì)胞趨化因子的表達(dá)及機(jī)制探討. 中國(guó)呼吸與危重監(jiān)護(hù)雜志, 2010, 9(5): 490-492. doi: 復(fù)制
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| 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(jìn)展. 中國(guó)呼吸與危重監(jiān)護(hù)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(jìn)展. 中國(guó)呼吸與危重監(jiān)護(hù)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.