İnsan barsağında gastrodüedonal hastalıklara yol açan Heliccobacter pylori'nin kalıcı kolonizasyonu

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.

Persistent colonization of Helicobacter pylori in human gut induces gastroduodenal diseases

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. .J Microbiol Infect Dis 2014; 4(4): 170-176

___

  • 1. Atherton JC. Thepathogenesis of Helicobacter pylori-induced gastro-duodenal diseases. Ann Rev Path 2006; 1: 63-96.
  • 2. Kusters JG, VanAH, Kuipers EJ. Pathogenesis of Helicobacter pylori infection. Clin Microbiol Rev 2006;19: 449-490.
  • 3. Tomb JF, White O, Kerlavage AR. The complete genome sequence of the gastric pathogen Helicobacter pylori. Nature 1997; 388: 539-547.
  • 4. Alm RA, Ling LS, Moir DT. Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori. Nature 1999; 397: 176-180.
  • 5. 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.
  • 6. Suerbaum S, Smith JM, Bapumia K. Free recombination within Helicobacter pylori. Proc Natl Acad Sci U S A 1998; 95: 12619-12624.
  • 7. Montecucco C, Papini E, Bernard M. Helicobacter pyloriVacAvacuolatingcytotoxin and HP-Nap neutrophil activating protein. Mol Cell Biol 2001;32:245-263.
  • 8. 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.
  • 9. Cao P, Cover TL, et al. Two different families of hopQ alleles in Helicobacter pylori. AmSocMicrobiol 2002; 40: 4504-4511.
  • 10. Nestorovich EM, BezrukovSM. Obstructing Toxin Pathways by Targeted Pore Blockage.ChemRev2012;112: 6388-6430.
  • 11. Domanska G, Motz C, Meinecke M, et al.Helicobacter pyloriVacA Toxin/Subunit p34: Targeting of an Anion Channel to the Inner Mitochondrial Membrane. PLo Patho 2010: 6: 41000878.
  • 12. Jaina P, Luob ZQ, Blankea SR.Helicobacter pylorivacuolatingcytotoxin A (VacA) engages the mitochondrial fission machinery to induce host cell death. PNAS 2011; 5: 1105175108.
  • 13. McClain MS, Cao P, Iwamoto H, et al.A 12-amino-acid segment, present in type S2 but not type S1 Helicobacter pyloriVacA proteins, abolishescytotoxin activity and alters membrane channel formation. J Bacteriol 2001; 183:6499-6508.
  • 14. Salama NR, Otto G, TompkinsL, Falkow S. Vacuolatingcytotoxin of Helicobacter pyloriplays a role during colonization in a mouse model of infection. Infect Immun 2001; 69: 730-736.
  • 15. Atherton JC, Peek RM, Tham KT, et al.Clinical and pathological importance of heterogeneity in vacA, the vacuolating cy-totoxin gene of Helicobacter pylori.Gastroenter1997; 112:92-101.
  • 16. CensiniS, Lange C, Xiang Z. Cag A pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors. Proc Natl Acad Sci. U S A 1996; 93: 14648-14653.
  • 17. Odenbreit S, Puls J, Sedlmaier B, et al. Translocation of Helicobacter pyloriCagA into gastric epithelial cells by type IV secretion.Science 2000; 287:1497-500.
  • 18. Higashi H, Tsutsum R, Muto S. SHP-2 tyrosine phosphatase as an intracellular target of Helicobacter pyloriCagA protein. Science 2002; 295: 683-689.
  • 19. Cover TL,BlaserMJ.Helicobacter pylori in health and disease. Gastroenter 2009; 136: 1863-1873.
  • 20. Yokoyama K, Higashi H, Ishikawa S, et al. Functional antagonism between Helicobacter pyloriCagA andvacuolating toxin VacA in control of the NFAT signaling pathway in gastric epithelial cells. Proc Natl Acad Sci U S A 2005;102: 9661-9666.
  • 21. Gerhard M, Lehn N, Neumayer N, et al. Clinical relevance of the Helicobacter pylori gene for blood-group antigenbindingadhesin. Proc Natl Acad Sci U S A 1999; 96: 12778-12783.
  • 22. Atherton JC, Tham KT, Peek RM, et al.Density of Helicobacter pyloriinfection in vivo as assessed by quantitative culture and histology. JInfectDis 1996;174:v552-556.
  • 23. 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 vacuolatingcytotoxinVacA. CellMicrobiol 2008; 26: 324-334.
  • 24. Xiao B, Liu Z, Li S, et al.Induction of microRNA-155 during Helicobacter pylori Infection and Its Negative Regulatory Role in the Inflammatory Response. J Infect Dis 2009; 200:916-925.
  • 25. Newton K, Dixit VM.Signaling in Innate Immunity and Inflammation.Cold Spring Harbor 2012; 4: 006049.
  • 26. Krishnan J, Basith S, Choi S. Advances in Toll-like Receptor Signaling. Adv Sys Biol 2012; 1: 1 5-15.
  • 27. 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.
  • 28. Tili E, MichailleJ, CiminoA. Modulation of miR-155 and miR- 125b levels followinglipopolysaccharide/TNF-alpha stimulation and their possible roles in regulating the response to endotoxin shock. J Immunol 2006;179: 5082-5089.
  • 29. JiangJ, LeeE, SchmittgenT.Increased expression of microRNA-155inEpstein-Barrvirus transformed lymphoblastoid cell lines. GenChrom Can 2006; 45: 103-106. 30. Volinia S, Calin GA, Liu CG. A microRNA expression signature of human solid tumors defines cancer gene targets. Proc Natl Acad Sci USA 2006;103:2257-2261.
  • 31. CostineanS, ZanesiN, PekarskyY, Pre-Bcellproliferationandlymphoblasticleukemia/high-grade lymphoma in E(mu)- miR155 transgenic mice. Proc Natl Acad Sci USA 2006; 103: 7024-7029.
  • 32. Belair C, Darfeuille F, Staedel C. Helicobacter pylori and gastric cancer: possible role of microRNAs in this intimate relationship. Clin Microbiol Infect, 2009; 15:806-812
  • 33. Tili E, Michaille J, Cimino A. Modulation of miR-155 and miR- 125b levels following lipopolysaccharide/TNF-alpha stimulation and their possible roles in regulating the response to endotoxin shock. J Immunol 2007; 179: 5082-5091.
  • 34. Karin M, Lawrence T, Nizet V. Innate immunity gone awry: linking microbial infections to chronic inflammation and cancer. Cell 2006; 124: 823-835.
  • 35. Fujita S, ItoT, Mizutani T. miR-21GeneexpressiontriggeredbyAP-1issustainedthrougha double-negative feedback mechanism. J Mol Biol 2008;378:492-504.
  • 36. LofflerD, Brocke Heidrich K, Pfeifer G. Interleukin-6dependentsurvivalofmultiple myeloma cells involves the Stat3-mediated induction of microRNA-21 through a highly conserved enhancer. Blood 2007; 110: 1330-1333.
  • 37. ZhangZ, LiZ, GaoC. miR-21 play pivotal role in gastric cancer pathogenesis and progression. Lab Invest 2008;88: 1358- 1366.
  • 38. LiuT, TangH, LangY, et al. MicroRNA-27afunctionsasanoncogeneingastric adenocarcinoma by targeting prohibitin. Cancer Lett 2005; 273: 233-242.
  • 39. Mertens SU, Chintharlapalli S, Li X, et al.The oncogenic microRNA-27a targets genes that regulate specificity protein transcription factors and the G2-M checkpoint in MDAMB-231 breast cancer cells. Cancer Res 2007;67: 11001- 11011.
  • 40. Petrocca F, Viso ne R, Onelli MR. E2F1-regulated microRNAs impair TGFbeta-dependent cell-cycle arrest and apoptosis in gastric cancer. Cancer Cell 2008; 13: 272-286.
  • 41. 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.
  • 42. Petrocca F, Visone R, Rapazzotti M, et al. miR-106b and miR-93 decrease E2F1 expression, establish-ing a negative-feedback loop preventing E2F1 self-activation. Cancer Cell2008; 133: 272-286.
  • 43. He L, Thomson JM, Hemann MT. AmicroRNA polycistron as a potential human oncogene. Nature 2005; 435:828-833.
  • 44. Volinia S, Calin GA, Liu CG. A microRNA expression signature of human solid tumors defines cancer gene targets. Proc Natl Acad Sci USA 2006; 103: 2257-2261.
  • 45. Xiao C, Srinivasan L, Calado DP. Lymphoproliferative disease and autoimmunity in mice with increased miR-17-92 expression in lymphocytes. Nat Immunol 2008;9: 405-414.
  • 46. Kim Y, Yu J, Han T. Functional links between clustered microRNAs: suppression of cell-cycle inhibitors by microRNA clusters in gastric cancer. Nucl Ac Res 2009; 67: 367-373
  • 47. Wu W, Lee CW, Cho CH, et al.MicroRNA dysregulation in gastric cancer: a new player enters the game. Oncogen2010; 352: 1-11.
  • 48. Marshall BJ, Barrett C, Prakash R, et al.Urea protects Helicobacter (Campylobacter) pylori from the bactericidal effect of acid. Gastroent 1990; 99:697-702.
  • 49. Guillemin K, Noor R, Salama LS, Tompkins SF. Cagpathogenicity island-specific responses of gastric epithelial cells to Helicobacter pylori infection. Proc Natl Acad Sci USA 2002; 99:15136-15141.
  • 50. 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.
  • 51. Takeda K, Soon A.Toll receptors and pathogen resistance. CellMicrobiol 2003; 5:143-153.
  • 52. Aspinall GO, Monteiro MA. Lipopolysaccharides of Helicobacter pylori strains P466 and MO19: structures of the O antigen and core oligosaccharide regions. Biochem 1996; 35: 2498-2504.
  • 53. 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.
  • 54. Wunder C, Churin Y, Winau F, et al.Cholesterol glucosylation promotes immune evasion by Helicobacter pylori. Nat Med 2006;12:1030-1038.
  • 55. Algood HM, Torres D, UnutmazTL. Resistance ofprimary murine CD4+ T cells to Helicobacter pylorivacuolatingcytotoxin. Infect Immun 2007; 75:334-341.
  • 56. Zabaleta J, McGee AH, Zea CP, et al.Helicobacter pyloriarginase inhibits T cell proliferation and reduces the expression of the TCR zeta-chain (CD3). J Immunol 2004; 173:586-593.
  • 57. Wunder C, Churin Y, Winau F. Cholesterol glucosylation promotes immune evasion by Helicobacter pylori. Nat Med 2006; 12:1030-1038.
  • 58. Fox JG, Beck CA, Dangler MT, et al.Concurrent enteric helminth infection modu-lates inflammation and gastric immune responses and reduces Helicobacter induced gastric atrophy. Nat Med 2000; 6:536-542.
  • 59. Harris PR, Smythies LE, Smith PD, Dubois A. Inflammatory cytokinemRNA expression during early and persistent Helicobacter pylori infectionin nonhuman primates. J Infect Dis 2000; 181: 783-789.
  • 60. 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.
  • 61. Naumann M, Wessler S, Bartsch C. Activation of activator protein 1 and stress response kinases in epithelial cells colonized by Helicobacterpylori encoding the cag pathogenicity island. J Biol Chem 1999; 274:31655-31662.
  • 62. Higashi H, Tsutsumi R, Muto S, et al.SHP-2 tyrosine phosphatase as an intracellular target of Helicobacter pyloriCagA protein.Science2002; 295: 683-686.
  • 63. Higashi H, Nakaya A, Tsutsumi R, et al.Helicobacter pyloriCagA inducesRas-independent morphogenetic response through SHP-2 recruitment and activation. J BiolChem2004; 279:17205-17216.
  • 64. Yamac D, AyyildizT, Coskun U. Cyclooxygenase-2 expression and its association with angiogenesis, Helicobacter pylori, and clinicopathologic characteristics of gastric carcinoma.Pathol ResPract 2008; 204: 527-536.
  • 65. Li Q, Liu N, Shen B. Helicoba cter pylori enhances cyclooxygenase 2 expression via p38MAPK/ATF-2 signaling pathway in MKB45 cells. Cancer Lett 2009; 278:97-103.
  • 66. Yamac D, Ayyildiz T, Coşkun U, et al. Cyclooxygenase-2 expression and its association with angiogenesis, Helicobacter pylori, and clinicopathologic characteristics of gastric carcinoma.PatholResPract 2004;204: 527-536.
  • 67. Suerbaum S, Michetti P. Helicobacter pylori infection. N Engl J Med 2002; 347: 151175-1186.
Journal of Microbiology and Infectious Diseases-Cover
  • ISSN: 2146-3158
  • Başlangıç: 2011
  • Yayıncı: Sağlık Araştırmaları Derneği
Sayıdaki Diğer Makaleler

İran Kerman'da hastane kökenli Staphylococcus aureus suşlarında antimikrobiyalduyarlılık, virulans faktörleri ve biyofilm yapımı

Mohammad Reza SHAKİBAİE, Gholamabas SALAJEGHEH, Yasser GOLKARİ

Çin Guangdong Bölgesindeki bir üçüncü basamak hastanede izole karbapenem dirençli Enterobacteriaceae kökenlerinin moleküler özellikleri

Min LİU, Kang LİAO, Penghao GUO, Dongmei CHEN, Yili CHEN, Han HUANG, Yan ZENG

BOS'tan izole edilen pnömokok suşlarında penisilin direncinin artışı: Bir eğitim hastanesinden 15 yıllık tecrübe

Sevtap GÜRSOY, Gönül ŞENGÖZ, Filiz PEHLİVANOĞLU

Mycobacterium tuberculosis tanısında mikroskopi ve PCR metotlarının karşılaştırılması

Pooja SAXENA, Ashish K. ASTHANA, Molly MADAN

Febril nötropenik kanser hastalarında serum amiloid-A and C-reaktif protein CRP'nin enfeksiyon için öngörü değeri

Ayşe BATIREL, Serdar ÖZER, Taflan SALEPCİ, Serap GENCER

Miyelodisplastik sendromlu bir hastada Campylobacter fetus subsp. fetus'e bağlı bir bakteriyemi: Olgu sunumu

Hatice Türk DAĞI, Mehmet DAĞLI, Ayşe Rüveyda UĞUR, İnci TUNCER

Bu gerçekten bir erizipel mi?

İlker İnanç BALKAN, Muhammed BEKÇİBAŞI, Ayşe SALİHOĞLU, Ali MERT

İnsan barsağında gastrodüedonal hastalıklara yol açan Heliccobacter pylori'nin kalıcı kolonizasyonu

Animesh SARKER, Tasnim AHMED, Marufa NASREEN, Rafiad ISLAM, Rezual ISLAM, Noor JAHAN

Kedi tırmalaması sonrası Pasteurella multocida'ya bağlı abse: Olgu sunumu

Pınar KORKMAZ, Yeşim ALPAY, Nevil AYKIN, Figen ÇEVİK

Uzamış kolestazı olan akut hepatit A enfeksiyonunda steroid kullanımı

Meltem Işıkgöz TAŞBAKAN, Hasip KAHRAMAN, Bilgin Arda ARDA, Sercan ULUSOY, Tansu YAMAZHAN, Hüsnü PULLUKÇU, Oğuz Reşat SİPAHİ