• 1.四川大學華西醫(yī)院普外三科（成都 610041）;;
  • 2.四川大學華西醫(yī)院腫瘤生物治療國家重點實驗室;;
  • 3.四川大學華西醫(yī)院中西醫(yī)結合科;

目的探討人急性胰腺炎早期外周血單核細胞(peripheral blood monocytes,PBMCs)表面Toll樣受體4(Toll like receptor 4,TLR4)表達變化。
方法發(fā)病24 h內入院的早期急性胰腺炎患者30例，采集入院當天及第3、7 d外周血及20名正常志愿者外周血，分離單核細胞。用流式細胞儀檢測單核細胞表面TLR4、CD14表達變化情況。同時檢測血清腫瘤壞死因子-α（tumor necrosis factor alpha,TNF-α）、白細胞介素6（interleukin 6,IL-6）等指標，研究它們之間的相關性。
結果急性胰腺炎患者PBMCs表面TLR4發(fā)病后表達上調， 1周左右恢復正常。TNF-α的變化與TLR4變化一致。
結論人急性胰腺炎早期可能通過先天性免疫門戶蛋白TLR4激活單核巨噬細胞系統(tǒng)導致TNF-α等促炎細胞因子的產生和釋放。

引用本文： 李紅光,周總光,雷松,朱林,鄭雪蓮,張鴻彥,王永,張建成. 人急性胰腺炎早期外周血單核細胞Toll樣受體4表達變化. 中國普外基礎與臨床雜志, 2006, 13(2): 197-200. doi: 復制

版權信息： ?四川大學華西醫(yī)院華西期刊社《中國普外基礎與臨床雜志》版權所有，未經(jīng)授權不得轉載、改編

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28. Dybdahl B, Wahba A, Lien E, et al. Inflammatory response after open heart surgery: release of heatshock protein 70 and signaling through tolllike receptor4.
29. Li Y, Zhou ZG, Xia QJ, et al. Tolllike receptor 4 detected in exocrine pancreas and the change of expression in ceruleininduced pancreatitis.
30. Gotzinger P, Sautner T, Spittler A, et al. Severe acute pancreatitis causes alterations in HLADR and CD14 expression on peripheral blood monocytes independently of surgical treatment.
  1. 1. [Ｊ].Science, 2002; 296(5566)∶ 301.
  2. 2.
  3. 3.
  4. 4.
  5. 5. [Ｊ]. J Immunol， 2004; 172(1)∶20.
  6. 6.
  7. 7. [Ｊ]. Arch Surg, 1993; 128(5)∶586.
  8. 8.
  9. 9. [Ｊ]. J Surg Res, 1996; 63(1)∶369.
  10. 10. [Ｊ]. Am J Respir Crit Care Med, 2003; 168(2)∶148.
  11. 11. [Ｊ].Dig Dis Sci, 1997; 42(8)∶1783.
  12. 12.
  13. 13. [Ｊ].Gastroenterology, 1997; 113(5)∶1741.
  14. 14. [Ｊ]. Surgery, 2004; 135(4)∶376.
  15. 15. [Ｊ]. Circulation, 2002; 105(6)∶685.
  16. 16. [Ｊ]. Pancreas, 2005; 30(4)∶375.
  17. 17. [Ｊ]. Eur J Surg, 2000; 166(8)∶628.
  18. 18. Matzinger P. The danger model: a renewed sense of self.
  19. 19. Jaffray C, Yang J, Norman J. Elastase mimics pancreatitisinduced hepatic injury via inflammatory mediators [Ｊ]. J Surg Res, 2000; 90(2)∶95.
  20. 20. Murr MM, Yang J, Fier A, et al. Pancreatic elastase induces liver injury by activating cytokine production within Kupffer cells via nuclear factorKappa B [Ｊ]. J Gastrointest Surg, 2002; 6(3)∶474.
  21. 21. Johnson GB, Brunn GJ, Platt JL. Cutting edge: an endogenous pathway to systemic inflammatory response syndrome (SIRS)like reactions through Tolllike receptor 4.
  22. 22. Bradley EL 3rd. A clinically based classification system for acute pancreatitis. Summary of the International Symposium on Acute Pancreatitis, Atlanta, Ga, September 11 through 13, 1992.
  23. 23. Fink GW, Norman JG. Intrapancreatic interleukin1beta gene expression by specific leukocyte populations during acute pancreatitis.
  24. 24. Dugernier TL, Laterre PF, Wittebole X, et al. Compartmentalization of the inflammatory response during acute pancreatitis: correlation with local and systemic complications.
  25. 25. Norman JG, Fink GW, Denham W, et al. Tissuespecific cytokine production during experimental acute pancreatitis. A probable mechanism for distant organ dysfunction.
  26. 26. Denham W, Yang J, Fink G, et al. Gene targeting demonstrates additive detrimental effects of interleukin 1 and tumor necrosis factor during pancreatitis.
  27. 27. Ikushima H, Nishida T, Takeda K, et al. Expression of Tolllike receptors 2 and 4 is downregulated after operation.
  28. 28. Dybdahl B, Wahba A, Lien E, et al. Inflammatory response after open heart surgery: release of heatshock protein 70 and signaling through tolllike receptor4.
  29. 29. Li Y, Zhou ZG, Xia QJ, et al. Tolllike receptor 4 detected in exocrine pancreas and the change of expression in ceruleininduced pancreatitis.
  30. 30. Gotzinger P, Sautner T, Spittler A, et al. Severe acute pancreatitis causes alterations in HLADR and CD14 expression on peripheral blood monocytes independently of surgical treatment.