BibTex RIS Kaynak Göster

Persistent Colonization of Helicobacter pylori in Human Gut induces gastroduodenal diseases.

Yıl 2014, , 170 - 176, 01.12.2014

Animesh Sarker

https://doi.org/10.5799/ahinjs.02.2014.04.0164

Öz

Helicobacter pylori are gut bacteria colonize in the epithelial cell lining of the stomach and persist there for long du­ration. Around two-thirds of the world\'s populations are infected with H. pylori and cause more than 90 percent of ulcers. The development of persistent inflammation is the main cause of chronic gastritis that finally results in a severe consequence known as stomach cancer. Two major virulence factors cytotoxin-associated gene product (cagA) and the vacuolating toxin (vacA) are mostly investigated as their close association with gastric carcinoma. In this review, host im­munity against H. pylori infection and their evasion mechanism are intensely explored. It is the fact, that understanding pin point molecular mechanisms of any infection is critical to develop novel strategies to prevent pertinent diseases. .

Anahtar Kelimeler

vacA cagA miRNA COX-2 Gastric carcinoma ver.

Kaynakça

  • Atherton JC. Thepathogenesis of Helicobacter pylori-induced gastro-duodenal diseases. Ann Rev Path 2006; 1: 63-96.
  • Kusters JG, VanAH, Kuipers EJ. Pathogenesis of Helicobacter pylori infection. Clin Microbiol Rev 2006;19: 449-490.
  • Tomb JF, White O, Kerlavage AR. The complete genome se- quence of the gastric pathogen Helicobacter pylori. Nature 1997; 388: 539-547.
  • Alm RA, Ling LS, Moir DT. Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helico- bacter pylori. Nature 1999; 397: 176-180.
  • Falush D, Kraft C, Taylor NS. Recombination and mutation during long-term gastric colonization by Helicobacter pylori: estimates of clock rates, recombination size, and minimal age. Proc Natl Acad Sci U S A 2001; 98:15056-15061.
  • Suerbaum S, Smith JM, Bapumia K. Free recombination with- in Helicobacter pylori. Proc Natl Acad Sci U S A 1998; 95: 12619-12624.
  • Montecucco C, Papini E, Bernard M. Helicobacter pyloriVa- cAvacuolatingcytotoxin and HP-Nap neutrophil activating protein. Mol Cell Biol 2001;32:245-263.
  • Rivera CG, Algood HM, Jana N, et al. The intermediate region of Helicobacter pyloriVacA is a determinant of toxin potency in a Jurkat T cell assay. Am Soc Microbiol2012; 10: 1128- 1140.
  • Cao P, Cover TL, et al. Two different families of hopQ alleles in Helicobacter pylori. AmSocMicrobiol 2002; 40: 4504-4511.
  • Nestorovich EM, BezrukovSM. Obstructing Toxin Pathways by Targeted Pore Blockage.ChemRev2012;112: 6388-6430.
  • Domanska G, Motz C, Meinecke M, et al.Helicobacter py- loriVacA Toxin/Subunit p34: Targeting of an Anion Channel to the Inner Mitochondrial Membrane. PLo Patho 2010: 6: 41000878.
  • Jaina P, Luob ZQ, Blankea SR.Helicobacter pylorivacuolat- ingcytotoxin A (VacA) engages the mitochondrial fission ma- chinery to induce host cell death. PNAS 2011; 5: 1105175108.
  • McClain MS, Cao P, Iwamoto H, et al.A 12-amino-acid seg- ment, present in type S2 but not type S1 Helicobacter pylori- VacA proteins, abolishescytotoxin activity and alters mem- brane channel formation. J Bacteriol 2001; 183:6499-6508.
  • Salama NR, Otto G, TompkinsL, Falkow S. Vacuolatingcyto- toxin of Helicobacter pyloriplays a role during colonization in a mouse model of infection. Infect Immun 2001; 69: 730-736.
  • Atherton JC, Peek RM, Tham KT, et al.Clinical and patho- logical importance of heterogeneity in vacA, the vacuolat- ing cy-totoxin gene of Helicobacter pylori.Gastroenter1997; 112:92-101.
  • CensiniS, Lange C, Xiang Z. Cag A pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-as- sociated virulence factors. Proc Natl Acad Sci. U S A 1996; 93: 14648-14653.
  • Odenbreit S, Puls J, Sedlmaier B, et al. Translocation of He- licobacter pyloriCagA into gastric epithelial cells by type IV secretion.Science 2000; 287:1497-500.
  • Higashi H, Tsutsum R, Muto S. SHP-2 tyrosine phosphatase as an intracellular target of Helicobacter pyloriCagA protein. Science 2002; 295: 683-689.
  • Cover TL,BlaserMJ.Helicobacter pylori in health and disease. Gastroenter 2009; 136: 1863-1873.
  • Yokoyama K, Higashi H, Ishikawa S, et al. Functional antago- nism between Helicobacter pyloriCagA andvacuolating toxin VacA in control of the NFAT signaling pathway in gastric epi- thelial cells. Proc Natl Acad Sci U S A 2005;102: 9661-9666.
  • Gerhard M, Lehn N, Neumayer N, et al. Clinical relevance of the Helicobacter pylori gene for blood-group antigenbinding- adhesin. Proc Natl Acad Sci U S A 1999; 96: 12778-12783.
  • Atherton JC, Tham KT, Peek RM, et al.Density of Helico- bacter pyloriinfection in vivo as assessed by quantitative cul- ture and histology. JInfectDis 1996;174:v552-556.
  • Tegtmeyer N, ZableD, Schmidt D, et al.Importance of EGF receptor,HER2/Neu and Erk1/2 kinase signaling for host cell elongation and scattering induced by theHelicobacter pylori CagA protein: antagonistic effects of the vacuolatingcytotox- inVacA. CellMicrobiol 2008; 26: 324-334.
  • Xiao B, Liu Z, Li S, et al.Induction of microRNA-155 dur- ing Helicobacter pylori Infection and Its Negative Regula- tory Role in the Inflammatory Response. J Infect Dis 2009; 200:916-925.
  • Newton K, Dixit VM.Signaling in Innate Immunity and Inflam- mation.Cold Spring Harbor 2012; 4: 006049.
  • Krishnan J, Basith S, Choi S. Advances in Toll-like Receptor Signaling. Adv Sys Biol 2012; 1: 1 5-15.
  • O’Connell RM, Taganov KD, Boldin MP, et al. MicroRNA-155 is induced duringthe macrophage inflammatory response. Proc Natl Acad Sci USA 2007; 104: 1604-1609.
  • Tili E, MichailleJ, CiminoA. Modulation of miR-155 and miR- 125b levels followinglipopolysaccharide/TNF-alpha stimula- tion and their possible roles in regulating the response to endotoxin shock. J Immunol 2006;179: 5082-5089.
  • JiangJ, LeeE, SchmittgenT.Increased expression of microR- NA-155inEpstein-Barrvirus transformed lymphoblastoid cell lines. GenChrom Can 2006; 45: 103-106.
  • Volinia S, Calin GA, Liu CG. A microRNA expression signa- ture of human solid tumors defines cancer gene targets. Proc Natl Acad Sci USA 2006;103:2257-2261.
  • CostineanS, ZanesiN, PekarskyY, Pre-Bcellproliferation- andlymphoblasticleukemia/high-grade lymphoma in E(mu)- miR155 transgenic mice. Proc Natl Acad Sci USA 2006; 103: 7024-7029.
  • Belair C, Darfeuille F, Staedel C. Helicobacter pylori and gas- tric cancer: possible role of microRNAs in this intimate rela- tionship. Clin Microbiol Infect, 2009; 15:806-812
  • Tili E, Michaille J, Cimino A. Modulation of miR-155 and miR- 125b levels following lipopolysaccharide/TNF-alpha stimula- tion and their possible roles in regulating the response to endotoxin shock. J Immunol 2007; 179: 5082-5091.
  • Karin M, Lawrence T, Nizet V. Innate immunity gone awry: linking microbial infections to chronic inflammation and can- cer. Cell 2006; 124: 823-835.
  • Fujita S, ItoT, Mizutani T. miR-21Geneexpressiontriggeredby- AP-1issustainedthrougha double-negative feedback mecha- nism. J Mol Biol 2008;378:492-504.
  • LofflerD, Brocke Heidrich K, Pfeifer G. Interleukin-6depen- dentsurvivalofmultiple myeloma cells involves the Stat3-me- diated induction of microRNA-21 through a highly conserved enhancer. Blood 2007; 110: 1330-1333.
  • ZhangZ, LiZ, GaoC. miR-21 play pivotal role in gastric cancer pathogenesis and progression. Lab Invest 2008;88: 1358- 1366.
  • LiuT, TangH, LangY, et al. MicroRNA-27afunctionsasanonco- geneingastric adenocarcinoma by targeting prohibitin. Can- cer Lett 2005; 273: 233-242.
  • Mertens SU, Chintharlapalli S, Li X, et al.The oncogenic microRNA-27a targets genes that regulate specificity pro- tein transcription factors and the G2-M checkpoint in MDA- MB-231 breast cancer cells. Cancer Res 2007;67: 11001- 11011.
  • Petrocca F, Visone R, Onelli MR. E2F1-regulated microRNAs impair TGFbeta-dependent cell-cycle arrest and apoptosis in gastric cancer. Cancer Cell 2008; 13: 272-286.
  • Petrocca F, Vecchione A, Croce CM. Emerging role of miR- 106b-25/miR-17-92 clusters in the control of transforming growth factor beta signaling. Cancer Res 2006; 68: 8191- 8194.
  • Petrocca F, Visone R, Rapazzotti M, et al. miR-106b and miR-93 decrease E2F1 expression, establish-ing a nega- tive-feedback loop preventing E2F1 self-activation. Cancer Cell2008; 133: 272-286.
  • He L, Thomson JM, Hemann MT. AmicroRNA polycistron as a potential human oncogene. Nature 2005; 435:828-833.
  • Volinia S, Calin GA, Liu CG. A microRNA expression signa- ture of human solid tumors defines cancer gene targets. Proc Natl Acad Sci USA 2006; 103: 2257-2261.
  • Xiao C, Srinivasan L, Calado DP. Lymphoproliferative dis- ease and autoimmunity in mice with increased miR-17-92 expression in lymphocytes. Nat Immunol 2008;9: 405-414.
  • Kim Y, Yu J, Han T. Functional links between clustered mi- croRNAs: suppression of cell-cycle inhibitors by microRNA clusters in gastric cancer. Nucl Ac Res 2009; 67: 367-373
  • Wu W, Lee CW, Cho CH, et al.MicroRNA dysregulation in gastric cancer: a new player enters the game. Oncogen2010; 352: 1-11.
  • Marshall BJ, Barrett C, Prakash R, et al.Urea protects Helico- bacter (Campylobacter) pylori from the bactericidal effect of acid. Gastroent 1990; 99:697-702.
  • Guillemin K, Noor R, Salama LS, Tompkins SF. Cagpatho- genicity island-specific responses of gastric epithelial cells to Helicobacter pylori infection. Proc Natl Acad Sci USA 2002; 99:15136-15141.
  • Guruge JL, Falk PG, Lorenz M, et al.Epithelial attachment alters the out-come of Helicobacter pylori infection. Proc Natl Acad Sci USA 1998; 95:3925-3930.
  • Takeda K, Soon A.Toll receptors and pathogen resistance. CellMicrobiol 2003; 5:143-153.
  • Aspinall GO, Monteiro MA. Lipopolysaccharides of Helico- bacter pylori strains P466 and MO19: structures of the O an- tigen and core oligosaccharide regions. Biochem 1996; 35: 2498-2504.
  • Jonsson K, Guo BP, Monstein HJ, Mekalanos JJ. Molecular cloning and characterization of two Helicobacter pylori genes coding for plasminogen-binding proteins.ProcNatl Acad Sci USA 2004; 101:1852-1858.
  • Wunder C, Churin Y, Winau F, et al.Cholesterol glucosylation promotes immune evasion by Helicobacter pylori. Nat Med 2006;12:1030-1038.
  • Algood HM, Torres D, UnutmazTL. Resistance ofprimary mu- rine CD4+ T cells to Helicobacter pylorivacuolatingcytotoxin. Infect Immun 2007; 75:334-341.
  • Zabaleta J, McGee AH, Zea CP, et al.Helicobacter pyloriargi- nase inhibits T cell proliferation and reduces the expression of the TCR zeta-chain (CD3). J Immunol 2004; 173:586-593.
  • Wunder C, Churin Y, Winau F. Cholesterol glucosylation promotes immune evasion by Helicobacter pylori. Nat Med 2006; 12:1030-1038.
  • Fox JG, Beck CA, Dangler MT, et al.Concurrent enteric hel- minth infection modu-lates inflammation and gastric immune responses and reduces Helicobacter induced gastric atro- phy. Nat Med 2000; 6:536-542.
  • Harris PR, Smythies LE, Smith PD, Dubois A. Inflammatory cytokinemRNA expression during early and persistent Heli- cobacter pylori infectionin nonhuman primates. J Infect Dis 2000; 181: 783-789.
  • Fischer W, Puo L, Buhrdorf R, et al. Systematic mutagenesis of the Helicobacter pylori cag pathogenicity island: essential genes for CagA translocation in host cells and induction of interleukin-8. Mol Microbiol 2001; 42:1337-1348.
  • Naumann M, Wessler S, Bartsch C. Activation of activator protein 1 and stress response kinases in epithelial cells colo- nized by Helicobacterpylori encoding the cag pathogenicity island. J Biol Chem 1999; 274:31655-31662.
  • Higashi H, Tsutsumi R, Muto S, et al.SHP-2 tyrosine phos- phatase as an intracellular target of Helicobacter pyloriCagA protein.Science2002; 295: 683-686.
  • Higashi H, Nakaya A, Tsutsumi R, et al.Helicobacter pylori- CagA inducesRas-independent morphogenetic response through SHP-2 recruitment and activation. J BiolChem2004; 279:17205-17216.
  • Yamac D, AyyildizT, Coskun U. Cyclooxygenase-2 expres- sion and its association with angiogenesis, Helicobacter pylori, and clinicopathologic characteristics of gastric carci- noma.Pathol ResPract 2008; 204: 527-536.
  • Li Q, Liu N, Shen B. Helicobacter pylori enhances cyclooxy- genase 2 expression via p38MAPK/ATF-2 signaling pathway in MKB45 cells. Cancer Lett 2009; 278:97-103.
  • Yamac D, Ayyildiz T, Coşkun U, et al. Cyclooxygenase-2 ex- pression and its association with angiogenesis, Helicobacter pylori, and clinicopathologic characteristics of gastric carci- noma.PatholResPract 2004;204: 527-536.
  • Suerbaum S, Michetti P. Helicobacter pylori infection. N Engl J Med 2002; 347: 151175-1186.

Persistent Colonization of Helicobacter pylori in Human Gut induces gastroduodenal diseases.

Yıl 2014, , 170 - 176, 01.12.2014

Animesh Sarker

https://doi.org/10.5799/ahinjs.02.2014.04.0164

Öz

Helicobacter pylori midenin epitelyal hücre hattında kolonize olan bir barsak bakterisi olup burada uzun süre sebat eder. Dünya nüfusunun yaklaşık üçte ikisi H. pylori ile enfektedir ve ülserlerin % 90’ından fazlasının etkenidir. Devamlı enflamasyonun gelişmesi kronik gastritin başlıca sebebidir ve nihai olarak mide kanseri olarak bilinen ciddi sonuçlara yol açabilir. Mide karsinomu ile yakından ilişkili olan sitokine eşlik eden gen ürünü (cagA) ve vakuoleştirici toksin (vacA) en fazla araştırılan iki major virulans faktörüdür. Bu derlemede H. pylori’ye karşı konak immünitesi ve onların kurtulma mekanizmaları yoğun şekilde açıklandı. Gerçektende bir enfeksiyonun bağlanmasındaki moleküler mekanizmasını anlamak korunma için yeni stratejiler geliştirmede kritik öneme sahiptir

Anahtar Kelimeler

vacA cagA miRNA COX-2 Mide karsinomu

Kaynakça

  • Atherton JC. Thepathogenesis of Helicobacter pylori-induced gastro-duodenal diseases. Ann Rev Path 2006; 1: 63-96.
  • Kusters JG, VanAH, Kuipers EJ. Pathogenesis of Helicobacter pylori infection. Clin Microbiol Rev 2006;19: 449-490.
  • Tomb JF, White O, Kerlavage AR. The complete genome se- quence of the gastric pathogen Helicobacter pylori. Nature 1997; 388: 539-547.
  • Alm RA, Ling LS, Moir DT. Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helico- bacter pylori. Nature 1999; 397: 176-180.
  • Falush D, Kraft C, Taylor NS. Recombination and mutation during long-term gastric colonization by Helicobacter pylori: estimates of clock rates, recombination size, and minimal age. Proc Natl Acad Sci U S A 2001; 98:15056-15061.
  • Suerbaum S, Smith JM, Bapumia K. Free recombination with- in Helicobacter pylori. Proc Natl Acad Sci U S A 1998; 95: 12619-12624.
  • Montecucco C, Papini E, Bernard M. Helicobacter pyloriVa- cAvacuolatingcytotoxin and HP-Nap neutrophil activating protein. Mol Cell Biol 2001;32:245-263.
  • Rivera CG, Algood HM, Jana N, et al. The intermediate region of Helicobacter pyloriVacA is a determinant of toxin potency in a Jurkat T cell assay. Am Soc Microbiol2012; 10: 1128- 1140.
  • Cao P, Cover TL, et al. Two different families of hopQ alleles in Helicobacter pylori. AmSocMicrobiol 2002; 40: 4504-4511.
  • Nestorovich EM, BezrukovSM. Obstructing Toxin Pathways by Targeted Pore Blockage.ChemRev2012;112: 6388-6430.
  • Domanska G, Motz C, Meinecke M, et al.Helicobacter py- loriVacA Toxin/Subunit p34: Targeting of an Anion Channel to the Inner Mitochondrial Membrane. PLo Patho 2010: 6: 41000878.
  • Jaina P, Luob ZQ, Blankea SR.Helicobacter pylorivacuolat- ingcytotoxin A (VacA) engages the mitochondrial fission ma- chinery to induce host cell death. PNAS 2011; 5: 1105175108.
  • McClain MS, Cao P, Iwamoto H, et al.A 12-amino-acid seg- ment, present in type S2 but not type S1 Helicobacter pylori- VacA proteins, abolishescytotoxin activity and alters mem- brane channel formation. J Bacteriol 2001; 183:6499-6508.
  • Salama NR, Otto G, TompkinsL, Falkow S. Vacuolatingcyto- toxin of Helicobacter pyloriplays a role during colonization in a mouse model of infection. Infect Immun 2001; 69: 730-736.
  • Atherton JC, Peek RM, Tham KT, et al.Clinical and patho- logical importance of heterogeneity in vacA, the vacuolat- ing cy-totoxin gene of Helicobacter pylori.Gastroenter1997; 112:92-101.
  • CensiniS, Lange C, Xiang Z. Cag A pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-as- sociated virulence factors. Proc Natl Acad Sci. U S A 1996; 93: 14648-14653.
  • Odenbreit S, Puls J, Sedlmaier B, et al. Translocation of He- licobacter pyloriCagA into gastric epithelial cells by type IV secretion.Science 2000; 287:1497-500.
  • Higashi H, Tsutsum R, Muto S. SHP-2 tyrosine phosphatase as an intracellular target of Helicobacter pyloriCagA protein. Science 2002; 295: 683-689.
  • Cover TL,BlaserMJ.Helicobacter pylori in health and disease. Gastroenter 2009; 136: 1863-1873.
  • Yokoyama K, Higashi H, Ishikawa S, et al. Functional antago- nism between Helicobacter pyloriCagA andvacuolating toxin VacA in control of the NFAT signaling pathway in gastric epi- thelial cells. Proc Natl Acad Sci U S A 2005;102: 9661-9666.
  • Gerhard M, Lehn N, Neumayer N, et al. Clinical relevance of the Helicobacter pylori gene for blood-group antigenbinding- adhesin. Proc Natl Acad Sci U S A 1999; 96: 12778-12783.
  • Atherton JC, Tham KT, Peek RM, et al.Density of Helico- bacter pyloriinfection in vivo as assessed by quantitative cul- ture and histology. JInfectDis 1996;174:v552-556.
  • Tegtmeyer N, ZableD, Schmidt D, et al.Importance of EGF receptor,HER2/Neu and Erk1/2 kinase signaling for host cell elongation and scattering induced by theHelicobacter pylori CagA protein: antagonistic effects of the vacuolatingcytotox- inVacA. CellMicrobiol 2008; 26: 324-334.
  • Xiao B, Liu Z, Li S, et al.Induction of microRNA-155 dur- ing Helicobacter pylori Infection and Its Negative Regula- tory Role in the Inflammatory Response. J Infect Dis 2009; 200:916-925.
  • Newton K, Dixit VM.Signaling in Innate Immunity and Inflam- mation.Cold Spring Harbor 2012; 4: 006049.
  • Krishnan J, Basith S, Choi S. Advances in Toll-like Receptor Signaling. Adv Sys Biol 2012; 1: 1 5-15.
  • O’Connell RM, Taganov KD, Boldin MP, et al. MicroRNA-155 is induced duringthe macrophage inflammatory response. Proc Natl Acad Sci USA 2007; 104: 1604-1609.
  • Tili E, MichailleJ, CiminoA. Modulation of miR-155 and miR- 125b levels followinglipopolysaccharide/TNF-alpha stimula- tion and their possible roles in regulating the response to endotoxin shock. J Immunol 2006;179: 5082-5089.
  • JiangJ, LeeE, SchmittgenT.Increased expression of microR- NA-155inEpstein-Barrvirus transformed lymphoblastoid cell lines. GenChrom Can 2006; 45: 103-106.
  • Volinia S, Calin GA, Liu CG. A microRNA expression signa- ture of human solid tumors defines cancer gene targets. Proc Natl Acad Sci USA 2006;103:2257-2261.
  • CostineanS, ZanesiN, PekarskyY, Pre-Bcellproliferation- andlymphoblasticleukemia/high-grade lymphoma in E(mu)- miR155 transgenic mice. Proc Natl Acad Sci USA 2006; 103: 7024-7029.
  • Belair C, Darfeuille F, Staedel C. Helicobacter pylori and gas- tric cancer: possible role of microRNAs in this intimate rela- tionship. Clin Microbiol Infect, 2009; 15:806-812
  • Tili E, Michaille J, Cimino A. Modulation of miR-155 and miR- 125b levels following lipopolysaccharide/TNF-alpha stimula- tion and their possible roles in regulating the response to endotoxin shock. J Immunol 2007; 179: 5082-5091.
  • Karin M, Lawrence T, Nizet V. Innate immunity gone awry: linking microbial infections to chronic inflammation and can- cer. Cell 2006; 124: 823-835.
  • Fujita S, ItoT, Mizutani T. miR-21Geneexpressiontriggeredby- AP-1issustainedthrougha double-negative feedback mecha- nism. J Mol Biol 2008;378:492-504.
  • LofflerD, Brocke Heidrich K, Pfeifer G. Interleukin-6depen- dentsurvivalofmultiple myeloma cells involves the Stat3-me- diated induction of microRNA-21 through a highly conserved enhancer. Blood 2007; 110: 1330-1333.
  • ZhangZ, LiZ, GaoC. miR-21 play pivotal role in gastric cancer pathogenesis and progression. Lab Invest 2008;88: 1358- 1366.
  • LiuT, TangH, LangY, et al. MicroRNA-27afunctionsasanonco- geneingastric adenocarcinoma by targeting prohibitin. Can- cer Lett 2005; 273: 233-242.
  • Mertens SU, Chintharlapalli S, Li X, et al.The oncogenic microRNA-27a targets genes that regulate specificity pro- tein transcription factors and the G2-M checkpoint in MDA- MB-231 breast cancer cells. Cancer Res 2007;67: 11001- 11011.
  • Petrocca F, Visone R, Onelli MR. E2F1-regulated microRNAs impair TGFbeta-dependent cell-cycle arrest and apoptosis in gastric cancer. Cancer Cell 2008; 13: 272-286.
  • Petrocca F, Vecchione A, Croce CM. Emerging role of miR- 106b-25/miR-17-92 clusters in the control of transforming growth factor beta signaling. Cancer Res 2006; 68: 8191- 8194.
  • Petrocca F, Visone R, Rapazzotti M, et al. miR-106b and miR-93 decrease E2F1 expression, establish-ing a nega- tive-feedback loop preventing E2F1 self-activation. Cancer Cell2008; 133: 272-286.
  • He L, Thomson JM, Hemann MT. AmicroRNA polycistron as a potential human oncogene. Nature 2005; 435:828-833.
  • Volinia S, Calin GA, Liu CG. A microRNA expression signa- ture of human solid tumors defines cancer gene targets. Proc Natl Acad Sci USA 2006; 103: 2257-2261.
  • Xiao C, Srinivasan L, Calado DP. Lymphoproliferative dis- ease and autoimmunity in mice with increased miR-17-92 expression in lymphocytes. Nat Immunol 2008;9: 405-414.
  • Kim Y, Yu J, Han T. Functional links between clustered mi- croRNAs: suppression of cell-cycle inhibitors by microRNA clusters in gastric cancer. Nucl Ac Res 2009; 67: 367-373
  • Wu W, Lee CW, Cho CH, et al.MicroRNA dysregulation in gastric cancer: a new player enters the game. Oncogen2010; 352: 1-11.
  • Marshall BJ, Barrett C, Prakash R, et al.Urea protects Helico- bacter (Campylobacter) pylori from the bactericidal effect of acid. Gastroent 1990; 99:697-702.
  • Guillemin K, Noor R, Salama LS, Tompkins SF. Cagpatho- genicity island-specific responses of gastric epithelial cells to Helicobacter pylori infection. Proc Natl Acad Sci USA 2002; 99:15136-15141.
  • Guruge JL, Falk PG, Lorenz M, et al.Epithelial attachment alters the out-come of Helicobacter pylori infection. Proc Natl Acad Sci USA 1998; 95:3925-3930.
  • Takeda K, Soon A.Toll receptors and pathogen resistance. CellMicrobiol 2003; 5:143-153.
  • Aspinall GO, Monteiro MA. Lipopolysaccharides of Helico- bacter pylori strains P466 and MO19: structures of the O an- tigen and core oligosaccharide regions. Biochem 1996; 35: 2498-2504.
  • Jonsson K, Guo BP, Monstein HJ, Mekalanos JJ. Molecular cloning and characterization of two Helicobacter pylori genes coding for plasminogen-binding proteins.ProcNatl Acad Sci USA 2004; 101:1852-1858.
  • Wunder C, Churin Y, Winau F, et al.Cholesterol glucosylation promotes immune evasion by Helicobacter pylori. Nat Med 2006;12:1030-1038.
  • Algood HM, Torres D, UnutmazTL. Resistance ofprimary mu- rine CD4+ T cells to Helicobacter pylorivacuolatingcytotoxin. Infect Immun 2007; 75:334-341.
  • Zabaleta J, McGee AH, Zea CP, et al.Helicobacter pyloriargi- nase inhibits T cell proliferation and reduces the expression of the TCR zeta-chain (CD3). J Immunol 2004; 173:586-593.
  • Wunder C, Churin Y, Winau F. Cholesterol glucosylation promotes immune evasion by Helicobacter pylori. Nat Med 2006; 12:1030-1038.
  • Fox JG, Beck CA, Dangler MT, et al.Concurrent enteric hel- minth infection modu-lates inflammation and gastric immune responses and reduces Helicobacter induced gastric atro- phy. Nat Med 2000; 6:536-542.
  • Harris PR, Smythies LE, Smith PD, Dubois A. Inflammatory cytokinemRNA expression during early and persistent Heli- cobacter pylori infectionin nonhuman primates. J Infect Dis 2000; 181: 783-789.
  • Fischer W, Puo L, Buhrdorf R, et al. Systematic mutagenesis of the Helicobacter pylori cag pathogenicity island: essential genes for CagA translocation in host cells and induction of interleukin-8. Mol Microbiol 2001; 42:1337-1348.
  • Naumann M, Wessler S, Bartsch C. Activation of activator protein 1 and stress response kinases in epithelial cells colo- nized by Helicobacterpylori encoding the cag pathogenicity island. J Biol Chem 1999; 274:31655-31662.
  • Higashi H, Tsutsumi R, Muto S, et al.SHP-2 tyrosine phos- phatase as an intracellular target of Helicobacter pyloriCagA protein.Science2002; 295: 683-686.
  • Higashi H, Nakaya A, Tsutsumi R, et al.Helicobacter pylori- CagA inducesRas-independent morphogenetic response through SHP-2 recruitment and activation. J BiolChem2004; 279:17205-17216.
  • Yamac D, AyyildizT, Coskun U. Cyclooxygenase-2 expres- sion and its association with angiogenesis, Helicobacter pylori, and clinicopathologic characteristics of gastric carci- noma.Pathol ResPract 2008; 204: 527-536.
  • Li Q, Liu N, Shen B. Helicobacter pylori enhances cyclooxy- genase 2 expression via p38MAPK/ATF-2 signaling pathway in MKB45 cells. Cancer Lett 2009; 278:97-103.
  • Yamac D, Ayyildiz T, Coşkun U, et al. Cyclooxygenase-2 ex- pression and its association with angiogenesis, Helicobacter pylori, and clinicopathologic characteristics of gastric carci- noma.PatholResPract 2004;204: 527-536.
  • Suerbaum S, Michetti P. Helicobacter pylori infection. N Engl J Med 2002; 347: 151175-1186.
Toplam 67 adet kaynakça vardır.

Ayrıntılar

Birincil Dil İngilizce
Bölüm Derleme
Yazarlar

Animesh Sarker Bu kişi benim

Yayımlanma Tarihi 1 Aralık 2014
Yayımlandığı Sayı Yıl 2014

Kaynak Göster

APA Sarker, A. (2014). Persistent Colonization of Helicobacter pylori in Human Gut induces gastroduodenal diseases. Journal of Microbiology and Infectious Diseases, 4(04), 170-176. https://doi.org/10.5799/ahinjs.02.2014.04.0164
AMA Sarker A. Persistent Colonization of Helicobacter pylori in Human Gut induces gastroduodenal diseases. J Microbil Infect Dis. Aralık 2014;4(04):170-176. doi:10.5799/ahinjs.02.2014.04.0164
Chicago Sarker, Animesh. “Persistent Colonization of Helicobacter Pylori in Human Gut Induces Gastroduodenal Diseases”. Journal of Microbiology and Infectious Diseases 4, sy. 04 (Aralık 2014): 170-76. https://doi.org/10.5799/ahinjs.02.2014.04.0164.
EndNote Sarker A (01 Aralık 2014) Persistent Colonization of Helicobacter pylori in Human Gut induces gastroduodenal diseases. Journal of Microbiology and Infectious Diseases 4 04 170–176.
IEEE A. Sarker, “Persistent Colonization of Helicobacter pylori in Human Gut induces gastroduodenal diseases”., J Microbil Infect Dis, c. 4, sy. 04, ss. 170–176, 2014, doi: 10.5799/ahinjs.02.2014.04.0164.
ISNAD Sarker, Animesh. “Persistent Colonization of Helicobacter Pylori in Human Gut Induces Gastroduodenal Diseases”. Journal of Microbiology and Infectious Diseases 4/04 (Aralık 2014), 170-176. https://doi.org/10.5799/ahinjs.02.2014.04.0164.
JAMA Sarker A. Persistent Colonization of Helicobacter pylori in Human Gut induces gastroduodenal diseases. J Microbil Infect Dis. 2014;4:170–176.
MLA Sarker, Animesh. “Persistent Colonization of Helicobacter Pylori in Human Gut Induces Gastroduodenal Diseases”. Journal of Microbiology and Infectious Diseases, c. 4, sy. 04, 2014, ss. 170-6, doi:10.5799/ahinjs.02.2014.04.0164.
Vancouver Sarker A. Persistent Colonization of Helicobacter pylori in Human Gut induces gastroduodenal diseases. J Microbil Infect Dis. 2014;4(04):170-6.