期刊文献+

Helicobacter pylori upregulates prion protein expression in gastric mucosa: A possible link to prion disease 被引量:9

Helicobacter pylori upregulates prion protein expression in gastric mucosa: A possible link to prion disease
下载PDF
导出
摘要 AIM: Pathological prion protein (PrP^sc) is responsible for the development of transmissible spongiform encephalopathies (TSE). While PrPc enters the organism via the oral route, less data is available to know about its uptake and the role of gastrointestinal inflammation on the expression of priori precursor PrPc, which is constitutively expressed in the gastric mucosa.METHODS: We studied PrPc expression in the gastric mucosa of 10 Helicobacter pylori-positive patients before and after successful H pylori eradication compared to non-infected controls using RT-PCR and Western blotting. The effect of central mediators of gastric inflammation, i.e., gastrin, prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) on PrPc expression was analyzed in gastric cell lines.RESULTS: PrPc expression was increased in H pyloriinfection compared with non-infected controls and decreased to normal after successful eradication. Gastrin, PGE2, and IL-1β dose-dependently upregulated PrPc in gastric cells, while TNF-α had no effect.CONCLUSION: H pylori infection leads to the upregulation of gastric PrPc expression. This can be linked to H pylori induced hypergastrinemia and increased mucosal PGE2 and IL-1β synthesis. H pylori creates a milieu for enhanced propagation of prions in the gastrointestinal tract. AIM: Pathological prion protein (PrPSC) is responsible for the development of transmissible spongiform encephalopathies (TSE). While PrPc enters the organism via the oral route, less data is available to know about its uptake and the role of gastrointestinal inflammation on the expression of prion precursor PrPc, which is constitutively expressed in the gastric mucosa.METHODS: We studied PrPc expression in the gastric mucosa of 10 Helicobacter pylori-positive patients before and after successful H pylori eradication compared to non-infected controls using RT-PCR and Western blotting.The effect of central mediators of gastric inflammation,i.e., gastrin, prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) on PrPc expression was analyzed in gastric cell lines.RESULTS: PrPc expression was increased in H pyloriinfection compared with non-infected controls and decreased to normal after successful eradication. Gastrin,PGE2, and IL-1β dose-dependently upregulated PrPc in gastric cells, while TNF-α had no effect.CONCLUSION: H pylori infection leads to the upregulation of gastric PrPc expression. This can be linked to H pylori induced hypergastrinemia and increased mucosal PGE2 and IL-1β synthesis.H pylori creates a milieu for enhanced propagation of prions in the gastrointestinal tract.
机构地区 Department of Medicine
出处 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第48期7651-7656,共6页 世界胃肠病学杂志(英文版)
基金 Supported by Bavarian Ministry of Health, Germany
关键词 PRIONS Helicobacter pylori Gastrin Proinflammatory cytokines 幽门螺杆菌 细菌感染 基因表达 胃黏膜
  • 引文网络
  • 相关文献

参考文献34

  • 1[1]Prusiner SB.Prions.Proc Natl Acad Sci USA 1998; 95:13363-13383 被引量:1
  • 2[2]Raeber AJ,Brandner S,Klein MA,Benninger Y,Musahl C,Frigg R,Roeckl C,Fischer MB,Weissmann C,Aguzzi A.Transgenic and knockout mice in research on prion diseases.Brain Pathol 2002; 98:715-733 被引量:1
  • 3[3]Weissmann C,Bueler H,Fischer M,Sailer A,Aguzzi A,Aguet M.PrP-deficient mice are resistant to scrapie.Ann NY Acad Sci 1994; 724:235-240 被引量:1
  • 4[4]Beekes M,McBride PA.Early accumulation of pathological PrP in the enteric nervous system and gut-associated lymphoid tissue of hamsters orally infected with scrapie.Neurosci Lett 2000; 278:181-184 被引量:1
  • 5[5]Shmakov AN,Ghosh S.Prion proteins and the gut:une liaison dangereuse? Gut 2001; 48:443-447 被引量:1
  • 6[6]Shmakov AN,McLennan NF,McBride P,Farquhar CF,Bode J,Rennison KA,Ghosh S.Cellular prion protein is expressed in the human enteric nervous system.Nat Med 2000; 6:840-841 被引量:1
  • 7[7]Gauczynski S,Peyrin JM,Haik S,Leucht C,Hundt C,Rieger R,Krasemann S,Deslys JP,Dormont D,Lasmezas CI,Weiss S.The 37-kDa/67-kDa laminin receptor acts as the cell surface receptor for the cellular prion protein.EMBO J 2001; 20:5863-5875 被引量:1
  • 8[8]Rieger R,Edenhofer F,Lasmezas CI,Weiss S.The human 37-kDa laminin receptor precursor interacts with the prion protein in eucaryotic cells.Nature Med 1997; 3:383-1388 被引量:1
  • 9[9]Shmakov AN,Bode J,Kilshaw PJ,Ghosh S.Diverse patterns of expression of the 67-kD laminin receptor in human small intestinal mucosa:potential binding sites for prion proteins? J Pathol 2000; 191:318-322 被引量:1
  • 10[10]Heppner FL,C.A.,Klein MA,Prinz M,Fried M,Kraehenbuhl JP,Aguzzi A.Transepithelial prion transport by M cells.Nature Med 2001; 7:976-977 被引量:1

同被引文献38

引证文献9

二级引证文献20

;
使用帮助 返回顶部