SIGIRR 在人正常肺組織及在脂多糖誘導的肺泡上皮細胞急性損傷中的表達及意義_《中國呼吸與危重監護雜志》

作者：

田豐 , 王云杰 , 趙晉波 , 張志培 ,  姜濤

第四軍醫大學唐都醫院胸外科（陜西西安 710038）;

關鍵詞：

急性肺損傷單一免疫球蛋白白細胞介素1 受體相關蛋白肺泡上皮細胞

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目的檢測單一免疫球蛋白白細胞介素1 受體相關蛋白( SIGIRR) 在正常肺組織及脂多糖( LPS ) 誘導的肺泡上皮細胞急性損傷中的表達。方法收集手術切除的正常肺組織標本20 例,分別采用免疫組織化學、Western blot、RT-PCR 法檢測SIGIRR 的表達。以終濃度10 μg/mL的LPS 刺激人Ⅱ型肺泡上皮細胞來源的A549 細胞, 于刺激前, 刺激后3、6、12 及24 h 分別以Western blot 法檢測SIGIRR 表達的變化。將含有SIGIRR cDNA 全長的表達載體瞬時轉染A549 細胞, 使SIGIRR 在A549 細胞過表達。通過MTT 法檢測LPS 對A549 細胞的損傷作用。結果不同檢測方法發現SIGIRR 在正常肺組織中均有表達; 免疫組織化學檢測可見SIGIRR 表達于肺泡上皮細胞。LPS 刺激后3、6 及12 h 時SIGIRR 表達較刺激前均下調, 24 h后回升至刺激前水平。MTT 試驗表明過表達SIGIRR 的A549 細胞在接受LPS 刺激后生長抑制率顯著低于對照組。結論 SIGIRR 能夠表達于正常肺組織, 且能夠減輕LPS 刺激導致的肺泡上皮細胞損傷。提示SIGIRR 可能參與了LPS 誘導的ALI的調節。

引用本文： 田豐,王云杰,趙晉波,張志培,姜濤. SIGIRR 在人正常肺組織及在脂多糖誘導的肺泡上皮細胞急性損傷中的表達及意義. 中國呼吸與危重監護雜志, 2009, 09(3): 242-246. doi: 復制

1.	Thomassen E, Renshaw BR, Sims JE. Identification and characterization of SIGIRR, a molecule representing a novel subtype of the IL-1R superfamily. Cytokine, 1999, 11: 389-399.
2.	Qin J, Qian Y, Yao J, et al. SIGIRR inhibits interleukin-1 receptorand toll-like receptor 4-mediated signaling through different mechanisms. J Biol Chem, 2005, 280: 25233-25241.
3.	Wald D, Qin J, Zhao Z, et al. SIGIRR, a negative regulator of Tolllike receptor-interleukin 1 receptor signaling. Nat Immunol, 2003 ,4: 920-927.
4.	Garlanda C, Riva F, Veliz T, et al. Increased susceptibility to colitisassociated cancer of mice lacking TIR8, an inhibitory member of the interleukin-1 receptor family. Cancer Res, 2007, 67: 6017-6021.
5.	修清玉, 錢建美, 王桂芳, 等. 不可分型流感嗜血桿菌誘導A549 細胞分泌和表達前炎癥細胞因子及機制研究. 中國呼吸與危重監護雜志, 2008, 7: 210-213.
6.	Garlanda C, Di Liberto D, Vecchi A, et al. Damping excessive inflammation and tissue damage in Mycobacterium tuberculosis infection by Toll IL-1 receptor 8 / single Ig IL-1-related receptor, a negative regulator of IL-1 / TLR signaling. J Immunol, 2007, 179 :3119-3125.
7.	Adib-Conquy M, Adrie C, Fitting C, et al. Up-regulation of MyD88s and SIGIRR, molecules inhibiting Toll-like receptor signaling, in monocytes from septic patients. Crit Care Med, 2006 , 34: 2377 -2385.
8.	Rubenfeld GD, Caldwell E, Peabody E, et al. Incidence and outcomes of acute lung injury. N Engl J Med, 2005, 353: 1685-1693.
9.	Martin TR, Rubenfeld GD, Ruzinski JT, et al. Relationship between soluble CD14 , lipopolysaccharide binding protein, and the alveolar inflammatory response in patients with acute respiratory distress syndrome. AmJ Respir Crit Care Med, 1997, 155: 937-944.
10.	Brégeon F, Papazian L, Delpierre S, et al. Role of proinflammatory activity contained in gastric juice from intensive care unit patients to induce lung injury in a rabbit aspiration model. Crit Care Med,2008, 36: 3205-3212.
11.	Bastarache JA, Wang L, Geiser T, et al. The alveolar epithelium can initiate the extrinsic coagulation cascade through expression of tissue factor. Thorax, 2007, 62: 608-616.
12.	Donnarumma G, Paoletti I, Buommino E, et al. Anti-inflammatory effects of moxifloxacin and human beta-defensin 2 association in human lung epithelial cell line ( A549 ) stimulated with lipopolysaccharide. Peptides, 2007, 28: 2286-2292.
13.	Armstrong L, Medford AR, Uppington KM, et al. Expression of functional toll-like receptor-2 and -4 on alveolar epithelial cells. Am J Respir Cell Mol Biol, 2004, 31: 241-245.

1. Thomassen E, Renshaw BR, Sims JE. Identification and characterization of SIGIRR, a molecule representing a novel subtype of the IL-1R superfamily. Cytokine, 1999, 11: 389-399.
2. Qin J, Qian Y, Yao J, et al. SIGIRR inhibits interleukin-1 receptorand toll-like receptor 4-mediated signaling through different mechanisms. J Biol Chem, 2005, 280: 25233-25241.
3. Wald D, Qin J, Zhao Z, et al. SIGIRR, a negative regulator of Tolllike receptor-interleukin 1 receptor signaling. Nat Immunol, 2003 ,4: 920-927.
4. Garlanda C, Riva F, Veliz T, et al. Increased susceptibility to colitisassociated cancer of mice lacking TIR8, an inhibitory member of the interleukin-1 receptor family. Cancer Res, 2007, 67: 6017-6021.
5. 修清玉, 錢建美, 王桂芳, 等. 不可分型流感嗜血桿菌誘導A549 細胞分泌和表達前炎癥細胞因子及機制研究. 中國呼吸與危重監護雜志, 2008, 7: 210-213.
6. Garlanda C, Di Liberto D, Vecchi A, et al. Damping excessive inflammation and tissue damage in Mycobacterium tuberculosis infection by Toll IL-1 receptor 8 / single Ig IL-1-related receptor, a negative regulator of IL-1 / TLR signaling. J Immunol, 2007, 179 :3119-3125.
7. Adib-Conquy M, Adrie C, Fitting C, et al. Up-regulation of MyD88s and SIGIRR, molecules inhibiting Toll-like receptor signaling, in monocytes from septic patients. Crit Care Med, 2006 , 34: 2377 -2385.
8. Rubenfeld GD, Caldwell E, Peabody E, et al. Incidence and outcomes of acute lung injury. N Engl J Med, 2005, 353: 1685-1693.
9. Martin TR, Rubenfeld GD, Ruzinski JT, et al. Relationship between soluble CD14 , lipopolysaccharide binding protein, and the alveolar inflammatory response in patients with acute respiratory distress syndrome. AmJ Respir Crit Care Med, 1997, 155: 937-944.
10. Brégeon F, Papazian L, Delpierre S, et al. Role of proinflammatory activity contained in gastric juice from intensive care unit patients to induce lung injury in a rabbit aspiration model. Crit Care Med,2008, 36: 3205-3212.
11. Bastarache JA, Wang L, Geiser T, et al. The alveolar epithelium can initiate the extrinsic coagulation cascade through expression of tissue factor. Thorax, 2007, 62: 608-616.
12. Donnarumma G, Paoletti I, Buommino E, et al. Anti-inflammatory effects of moxifloxacin and human beta-defensin 2 association in human lung epithelial cell line ( A549 ) stimulated with lipopolysaccharide. Peptides, 2007, 28: 2286-2292.
13. Armstrong L, Medford AR, Uppington KM, et al. Expression of functional toll-like receptor-2 and -4 on alveolar epithelial cells. Am J Respir Cell Mol Biol, 2004, 31: 241-245.

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