Progression of Pathogenetic Research of Acute Pancreatitis_CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Authors：

YU Wen , WU Wei , ZHANG Shaohui , WANG Yaohua

Department of General Surgery, Dongfang Hospital， Beijing University of Chinese Medicine and Pharmacology， Beijing 100078, China;

Corresponding author：

Keywords：

Acute pancreatitis; Pathogenesis

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Objective　To summarize the recent pathogenetic researches on the acute pancreatitis. Methods　Relevant references about the pathogenesis of acute pancreatitis, which were published recently domestic and abroad were collected and reviewed. Results　Recent experimental data indicated that the synthesis and release of pro-inflammatory cytokines and chemotactic factors were responsible for local injury and systemic dissemination of the inflammatory mediators. Experimental studies also provided evidences implying that the immune system might play a role in the development of pancreatitis, such as the activation of lymphocyte and neutrophil. Additionally, the pancreas may completely recover or become fibrotic after an attack of acute pancreatitis and the presence of pancreatic stellate cell was known as a crucial factor in the fibrogenesis. Conclusion　The pathogenesis of acute pancreatitis is very complicated, the factors that determine the ultimate severity of the attack are still unknown.

Citation： YU Wen,WU Wei,ZHANG Shaohui,WANG Yaohua. Progression of Pathogenetic Research of Acute Pancreatitis. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2006, 13(6): 733-736. doi: Copy

1.	Raraty MG, Connor S, Criddle DN, et al. Acute pancreatitis and organ failure: pathophysiology, natural history, and management strategies [J]. Curr Gastroenterol Rep, 2004; 6(2)∶99.
2.	Gomez-Cambronero LG, Sabater L, Pereda J, et al. Role of cytokines and oxidative stress in the pathophysiology of acute pancreatitis: therapeutical implications [J]. Curr Drug Targets Inflamm Allergy, 2002; 1(4)∶393.
3.	Pastor CM, Frossard JL. Are genetically modified mice useful for the understanding of acute pancreatitis? [J].FASEB J, 2001; 15(6)∶893.
4.	Lerch MM, Saluja AK, Dawra R, et al. Acute necrotizing pancreatitis in the opossum: earliest morphological changes involve acinar cells [J]. Gastroenterology, 1992; 103(1)∶205.
5.	Altavilla D, Famulari C, Passaniti M, et al. Attenuated cerulein-induced pancreatitis in nuclear factor-kappaB-deficient mice [J]. Lab Invest, 2003; 83(12)∶1723.
6.	Hofbauer B, Saluja A, Lerch M, et al. Intra-acinar cell activation of trypsinogen during caerulein-induced pancreatitis in rats [J]. Am J Physiol, 1998; 275(2 Pt 1)∶G352.
7.	Steer ML, Meldolesi J, Figarella C. Pancreatitis. The role of lysosomes [J]. Dig Dis Sci, 1984; 29(10)∶934.
8.	De Lisle RC. Altered posttranslational processing of glycoproteins in cerulein-induced pancreatitis [J]. Exp Cell Res, 2005; 308(1)∶101.
9.	Halangk W, Lerch MM. Early events in acute pancreatitis [J].Clin Lab Med, 2005; 25(1)∶1.
10.	Van Acker GJ, Saluja AK, Bhagat L, et al. Cathepsin B inhibition prevents trypsinogen activation and reduces pancreatitis severity [J]. Am J Physiol Gastrointest Liver Physiol, 2002; 283(3)∶G794.
11.	Saluja AK, Bhagat L, Lee HS, et al. Secretagogue-induced digestive enzyme activation and cell injury in rat pancreatic acini [J]. Am J Physiol, 1999; 276(4 Pt 1)∶G835.
12.	Krajewski E, Krajewski J, Spodnik JH, et al. Changes in the morphology of the acinar cells of the rat pancreas in the oedematous and necrotic types of experimental acute pancreatitis [J]. Folia Morphol (Warsz), 2005; 64(4)∶292.
13.	Long J, Song N, Liu XP, et al. Nuclear factor-kappaB activation on the reactive oxygen species in acute necrotizing pancreatitic rats [J]. World J Gastroenterol, 2005; 11(27)∶4277.
14.	Jeyarajah DR, Kielar M, Gokaslan ST, et al. Fas deficiency exacerbates cerulein-induced pancreatitis [J]. J Invest Surg, 2003; 16(6)∶325.
15.	Bhatia M, Wallig MA, Hofbauer B, et al. Induction of apoptosis in pancreatic acinar cells reduces the severity of acute pancreatitis [J]. Biochem Biophys Res Commun, 1998; 246(2)∶476.
16.	Satoh A, Gukovskaya AS, Edderkaoui M, et al. Tumor necrosis factor-alpha mediates pancreatitis responses in acinar cells via protein kinase C and proline-rich tyrosine kinase 2 [J]. Gastroenterology, 2005; 129(2)∶639.
17.	Dobosz M, Hac S, Mionskowska L, et al. Organ microcirculatory disturbances in experimental acute pancreatitis. A role of nitric oxide [J]. Physiol Res, 2005; 54(4)∶363.
18.	Ranson JH, Rifkind KM, Roses DF, et al. Prognostic signs and the role of operative management in acute pancreatitis [J].Surg Gynecol Obstet, 1974; 139(1)∶69.
19.	Gloor B, Todd KE, Lane JS, et al. Hepatic Kupffer cell blockade reduces mortality of acute hemorrhagic pancreatitis in mice [J]. J Gastrointest Surg, 1998; 2(5)∶430.
20.	Pezzilli R, Billi P, Beltrandi E, et al. Impaired lymphocyte proliferation in human acute pancreatitis [J]. Digestion, 1997; 58(5)∶431.
21.	Demols A, Le Moine O, Desalle F, et al. CD4(+)T cells play an important role in acute experimental pancreatitis in mice [J].Gastroenterology, 2000; 118(3)∶582.
22.	Leindler L, Morschl E, Laszlo F, et al. Importance of cytokines, nitric oxide, and apoptosis in the pathological process of necrotizing pancreatitis in rats [J]. Pancreas, 2004; 29(2)∶157.
23.	Liu LR, Xia SH. Role of platelet-activating factor in the pathogenesis of acute pancreatitis [J]. World J Gastroenterol, 2006; 12(4)∶539.
24.	Warzecha Z, Dembinski A, Ceranowicz P, et al. IGF-1 stimulates production of interleukin-10 and inhibits development of caerulein-induced pancreatitis [J]. J Physiol Pharmacol, 2003; 54(4)∶575.
25.	Yoo BM, Yeo M, Oh TY, et al. Amelioration of pancreatic fibrosis in mice with defective TGF-beta signaling [J]. Pancreas, 2005; 30(3)∶e71.
26.	Kloppel G, Maillet B. The morphological basis for the evolution of acute pancreatitis into chronic pancreatitis [J].Virchows Arch A Pathol Anat Histopathol, 1992; 420(1)∶1.
27.	Sarles H. Alcoholism and pancreatitis [J]. Scand J Gastroenterol, 1971； 6（3）∶193.
28.	Shimizu K, Kobayashi M, Tahara J, et al. Cytokines and peroxisome proliferator-activated receptor gamma ligand regulate phagocytosis by pancreatic stellate cells [J]. Gastroenterology, 2005; 128(7)∶2105.
29.	Mews P, Phillips P, Fahmy R, et al. Pancreatic stellate cells respond to inflammatory cytokines: potential role in chronic pancreatitis [J]. Gut, 2002; 50(4)∶535.

1. 　Raraty MG, Connor S, Criddle DN, et al. Acute pancreatitis and organ failure: pathophysiology, natural history, and management strategies [J]. Curr Gastroenterol Rep, 2004; 6(2)∶99.
2. 　Gomez-Cambronero LG, Sabater L, Pereda J, et al. Role of cytokines and oxidative stress in the pathophysiology of acute pancreatitis: therapeutical implications [J]. Curr Drug Targets Inflamm Allergy, 2002; 1(4)∶393.
3. 　Pastor CM, Frossard JL. Are genetically modified mice useful for the understanding of acute pancreatitis? [J].FASEB J, 2001; 15(6)∶893.
4. 　Lerch MM, Saluja AK, Dawra R, et al. Acute necrotizing pancreatitis in the opossum: earliest morphological changes involve acinar cells [J]. Gastroenterology, 1992; 103(1)∶205.
5. 　Altavilla D, Famulari C, Passaniti M, et al. Attenuated cerulein-induced pancreatitis in nuclear factor-kappaB-deficient mice [J]. Lab Invest, 2003; 83(12)∶1723.
6. 　Hofbauer B, Saluja A, Lerch M, et al. Intra-acinar cell activation of trypsinogen during caerulein-induced pancreatitis in rats [J]. Am J Physiol, 1998; 275(2 Pt 1)∶G352.
7. 　Steer ML, Meldolesi J, Figarella C. Pancreatitis. The role of lysosomes [J]. Dig Dis Sci, 1984; 29(10)∶934.
8. 　De Lisle RC. Altered posttranslational processing of glycoproteins in cerulein-induced pancreatitis [J]. Exp Cell Res, 2005; 308(1)∶101.
9. 　Halangk W, Lerch MM. Early events in acute pancreatitis [J].Clin Lab Med, 2005; 25(1)∶1.
10. 　Van Acker GJ, Saluja AK, Bhagat L, et al. Cathepsin B inhibition prevents trypsinogen activation and reduces pancreatitis severity [J]. Am J Physiol Gastrointest Liver Physiol, 2002; 283(3)∶G794.
11. 　Saluja AK, Bhagat L, Lee HS, et al. Secretagogue-induced digestive enzyme activation and cell injury in rat pancreatic acini [J]. Am J Physiol, 1999; 276(4 Pt 1)∶G835.
12. 　Krajewski E, Krajewski J, Spodnik JH, et al. Changes in the morphology of the acinar cells of the rat pancreas in the oedematous and necrotic types of experimental acute pancreatitis [J]. Folia Morphol (Warsz), 2005; 64(4)∶292.
13. 　Long J, Song N, Liu XP, et al. Nuclear factor-kappaB activation on the reactive oxygen species in acute necrotizing pancreatitic rats [J]. World J Gastroenterol, 2005; 11(27)∶4277.
14. 　Jeyarajah DR, Kielar M, Gokaslan ST, et al. Fas deficiency exacerbates cerulein-induced pancreatitis [J]. J Invest Surg, 2003; 16(6)∶325.
15. 　Bhatia M, Wallig MA, Hofbauer B, et al. Induction of apoptosis in pancreatic acinar cells reduces the severity of acute pancreatitis [J]. Biochem Biophys Res Commun, 1998; 246(2)∶476.
16. 　Satoh A, Gukovskaya AS, Edderkaoui M, et al. Tumor necrosis factor-alpha mediates pancreatitis responses in acinar cells via protein kinase C and proline-rich tyrosine kinase 2 [J]. Gastroenterology, 2005; 129(2)∶639.
17. 　Dobosz M, Hac S, Mionskowska L, et al. Organ microcirculatory disturbances in experimental acute pancreatitis. A role of nitric oxide [J]. Physiol Res, 2005; 54(4)∶363.
18. 　Ranson JH, Rifkind KM, Roses DF, et al. Prognostic signs and the role of operative management in acute pancreatitis [J].Surg Gynecol Obstet, 1974; 139(1)∶69.
19. 　Gloor B, Todd KE, Lane JS, et al. Hepatic Kupffer cell blockade reduces mortality of acute hemorrhagic pancreatitis in mice [J]. J Gastrointest Surg, 1998; 2(5)∶430.
20. 　Pezzilli R, Billi P, Beltrandi E, et al. Impaired lymphocyte proliferation in human acute pancreatitis [J]. Digestion, 1997; 58(5)∶431.
21. 　Demols A, Le Moine O, Desalle F, et al. CD4(+)T cells play an important role in acute experimental pancreatitis in mice [J].Gastroenterology, 2000; 118(3)∶582.
22. 　Leindler L, Morschl E, Laszlo F, et al. Importance of cytokines, nitric oxide, and apoptosis in the pathological process of necrotizing pancreatitis in rats [J]. Pancreas, 2004; 29(2)∶157.
23. 　Liu LR, Xia SH. Role of platelet-activating factor in the pathogenesis of acute pancreatitis [J]. World J Gastroenterol, 2006; 12(4)∶539.
24. 　Warzecha Z, Dembinski A, Ceranowicz P, et al. IGF-1 stimulates production of interleukin-10 and inhibits development of caerulein-induced pancreatitis [J]. J Physiol Pharmacol, 2003; 54(4)∶575.
25. 　Yoo BM, Yeo M, Oh TY, et al. Amelioration of pancreatic fibrosis in mice with defective TGF-beta signaling [J]. Pancreas, 2005; 30(3)∶e71.
26. 　Kloppel G, Maillet B. The morphological basis for the evolution of acute pancreatitis into chronic pancreatitis [J].Virchows Arch A Pathol Anat Histopathol, 1992; 420(1)∶1.
27. 　Sarles H. Alcoholism and pancreatitis [J]. Scand J Gastroenterol, 1971； 6（3）∶193.
28. 　Shimizu K, Kobayashi M, Tahara J, et al. Cytokines and peroxisome proliferator-activated receptor gamma ligand regulate phagocytosis by pancreatic stellate cells [J]. Gastroenterology, 2005; 128(7)∶2105.
29. 　Mews P, Phillips P, Fahmy R, et al. Pancreatic stellate cells respond to inflammatory cytokines: potential role in chronic pancreatitis [J]. Gut, 2002; 50(4)∶535.

CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Progression of Pathogenetic Research of Acute Pancreatitis

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