遗传 ›› 2011, Vol. 33 ›› Issue (6): 558-566.doi: 10.3724/SP.J.1005.2011.00558
张丽1, 2, 王芃1 , 魏莎莉2 , 刘纯杰1
收稿日期:2010-09-30
修回日期:2011-01-14
出版日期:2011-06-20
发布日期:2011-06-25
通讯作者:
刘纯杰
E-mail:liucj@nic.bmi.ac.cn
基金资助:“十一五”国家863“疫苗与抗体工程”重大项目基金(编号：2006AA02A219),“十一五”国家“艾滋病和病毒性肝炎等重大传染病防治”重大专项基金(编号：2008ZX10004-015)和“十一五”国家科技支撑计划项目基金(编号：2008BAI66B03)资助
ZHANG Li1,2, WANG Peng1, WEI Sha-Li2, LIU Chun-Jie1
Received:2010-09-30
Revised:2011-01-14
Online:2011-06-20
Published:2011-06-25
Contact:
LIU Chun-Jie
E-mail:liucj@nic.bmi.ac.cn
摘要： 幽门螺杆菌(Helicobacter pylori)感染能导致慢性胃炎、消化性溃疡、胃粘膜相关的淋巴样组织 (Mu-cosa-associated lymphoid tissue, MALT)淋巴瘤和胃腺癌等疾病的发生。1994年世界卫生组织国际癌症研究中心(IARC)将H.pylori列为胃癌第一级因子。H.pylori感染引起的不同临床结局主要与H.pylori致病因子和宿主遗传易感性有关, 大部分重大疾病发生在特定的细菌毒力因子(如cagA, vacA)与易感宿主遗传背景共同存在时。文章综述了H.pylori菌株的毒力基因的分型和宿主的遗传多态性对胃病发生的影响。
张丽，王芃，魏莎莉，刘纯杰. 幽门螺杆菌毒力基因分型和宿主遗传多态性与胃病关系研究进展[J]. 遗传, 2011, 33(6): 558-566.
ZHANG Li, WANG Peng, WEI Sha-Chi, LIU Chun-Jie. Advances in relationship between gastric disease and polymorphisms in both helicobacter pylori virulence factors and host genetics[J]. HEREDITAS, 2011, 33(6): 558-566.
| [1] Rudi J, Kuck D, Rudy A, Sieg A, Maiwald M, Stremmel W. Helicobacter pylori vacA genotypes and cagA gene in a series of 383 H.pylori-positive patients. Z Gastroenterol, 2000, 38(7): 559-564.[2] Ahmad A, Govil Y, Frank BB. Gastric mucosa-associated lymphoid tissue lymphoma. Am J Gsatroenterol, 2003, 98(5): 975-986.[3] Olivares D, Gisbert JP. Factors involved in the pathogenesis of Helicobacter pylori infection. Rev Esp Enferm Dig, 2006, 98(5): 374-386.[4] Cover TL, Krishna US, Israel DA, Peek RM Jr. Induction of gastric epithelial cell apoptosis by Helicobacter pylori vacuolating cytotoxin. Cancer Res, 2003, 63(5): 951-957.[5] Covacci A, Censini S, Bugnoli M, Petracca R, Burroni D, Macchia G, Massone A, Papini E, Xiang Z, Figura N. Molecular characterization of the 128 kDa immunodominant antigen of Helicobacter pylori associated with cytotoxicity and duodenal ulcer. Proc Natl Acad Sci USA, 1993, 90(12): 5791-5795.[6] Peek RM Jr, Crabtree JE. Helicobacter infection and gastric neoplasia. J Pathol, 2006, 208(2): 233-248.[7] Ando T, Goto Y, Maeda O, Watanabe O, Ishiguro K, Goto H. Causal role of Helicobacter pylori infection in gastric cancer. World J Gastroenterol, 2006, 12(2): 181-186.[8] Crabtree JE, Covacci A, Farmery SM, Xiang Z, Tompkins DS, Perry S, Lindley IJ, Rappuoli R. Helicobacter pylori induced interleukin-8 expression in gastric epithelial cells is associated with CagA positive phenotype. J Clin Pathol, 1995, 48(1): 41-45.[9] Crabtree JE, Farmery SM, Lindley IJ, Figura N, Peichl P, Tompkins DS. CagA/cytotoxic strains of Helicobacter pylori and interleukin-8 in gastric epithelial cell lines. J Clin Pathol, 1994, 47(10): 945-950.[10] Sharma SA, Tummuru MK, Miller GG, Blaser MJ. Inter-leukin-8 response of gastric epithelial cell lines to Helicobacter pylori stimulation in vitro. Infect Immun, 1995, 63(5): 1681-1687.[11] Yamaoka Y, Kita M, Kodama T, Sawai N, Imanishi J. Helicobacter pylori cagA gene and expression of cytokine messenger RNA in gastric mucosa. Gastroenterology, 1996, 110(6): 1744-1752.[12] Peek RM, Miller GG, Tham KT, Perez-Perez GI, Zhao XM, Atherton JC, Blaser J. Heightened inflammatory response and cytokine expression in vivo to cagA+ Helicobacter pylori strains. Lab Invest, 1995, 73(6): 760-770.[13] Crabtree JE, Taylor JD, Wyatt JI, Heatley RV, Shallcross TM, Tompkins DS, Rathbone BJ. Mucosal IgA recognition of Helicobacter pylori 120 kDa protein, peptic ulceration, and gastric pathology. Lancet, 1991, 338(8763): 332-335.[14] Weel JFL, van der Hulst RWM, Gerrits Y, Roorda P, Feller M, Dankert J, Tytgat GNJ, van der Ende A. The interrela-tionship between cytotoxin-associated gene A, vacuolating cytotoxin, and Helicobacter pylori-related diseases. J Infect Dis, 1996, 173(5): 1171-1175.[15] Parsonnet J, Friedman GD, Orentreich N, Vogelman H. Risk for gastric cancer in people with CagA positive or CagA negative Helicobacter pylori infection. Gut, 1997, 40(3): 297-301.[16] Blaser MJ, Perez-Perez GI, Kleanthous H, Cover TL, Peek RM, Chyou PH, Stemmermann GN, Nomura A. Infection with Helicobacter pylori strains possessing cagA is associated with an increased risk of developing adenocarcinoma of the stomach. Cancer Res, 1995, 55(10): 2111-2115.[17] Crabtree JE, Wyatt JI, Sobala GM, Miller G, Tompkins DS, Primrose JN, Morgan AG. Systemic and mucosal humoral responses to Helicobacter pylori in gastric cancer. Gut, 1993, 34(10): 1339-1343.[18] Li J, Ou ZY, Wang FJ, Guo Y, Zhang R, Zhang J, Li PQ, Xu WJ, He YS. Distinctiveness of the cagA geno-type in children and adults with peptic symptoms in South China. Helicobacter, 2009, 14(4): 248-255.[19] Tummuru MK, Sharma SA, Blaser MJ. Helicobacter pylori picB, a homologue of the Bordetella pertussis toxin secretion protein, is required for induction of IL-8 in gastric epithelial cells. Mol Microbiol, 1995, 18(5): 867-876.[20] Covacci A, Telford JL, Del Giudice G, Parsonnet J, Rappuoli R. Helicobacter pylori virulence and genetic geography. Science, 1999, 284(5418): 1328-1333.[21] Módena JLP, Sales AIL, Acrani GO, Russo R, Ribeiro MAV, Fukuhara Y, da Silveira WD, Módena JLP, de Oliveira RB, Brocchi M. Association between Helicobacter pylori genotypes and gastric disorders in relation to the cag pathogenicity island. Diagn Microbiol Infect Dis, 2007, 59(1): 7-16.[22] Amieva MR, EIOmar EM. Host-bacterial interaction in Helicobacter pylori infection. Gastroenterology, 2008, 134(1): 306-323.[23] Atherton JC, Cao P, Peek RM Jr, Tummuru MKR, Blaser MJ, Cover TL. Mosaicism in vacuolating cytotoxin alleles of Helicobacter pylori. Association of specific vacA types with cytotoxin production and peptic ulceration. J Biol Chem, 1995, 270(30): 17771-17777.[24] Blaser MJ, Atherton JC. Helicobacter pylori persistence: biology and disease. J Clin Invest, 2004, 113(3): 321-333.[25] Sugimoto M, Yamaoka Y. The association of vacA genotype and Helicobacter pylori-related disease in Latin American and African populations. Clin Microbiol Infect, 2009, 15(9): 835-842.[26] Bindayna KM, Al Mahmeed A. vacA genotypes in Helicobacter pylori strains isolated from patients with and without duodenal ulcer in Bahrain. Indian J Gastroenterol, 2009, 28(5): 179-175.[27] Douraghi M, Talebkhan Y, Zeraati H, Ebrahimzadeh F, Nahvijoo A, Morakabati A, Ghafarpour M, Esmaili M, Bababeik M, Oghalaie A, Rakhshani N, Hosseini ME, Mohagheghi MA, Mohammadi M. Multiple gene status in Helicobacter pylori strains and risk of gastric cancer development. Digestion, 2009, 80(3): 200-207.[28] Shirasaka D. Helicobacter pylori VacA and gastric ulcer. Int J Hematol, 2006, 84(4): 316-318.[29] Terebiznik MR, Vazquez CL, Torbicki K, Bans D, Wang T, Hong W, Blanke SR, Colombo MI, Jones NL. Helicobacter pylori VacA toxin promotes bacterial intracellular survival in gastric epithelial cells. Infect Immun 2006, 74(12): 6599-6614.[30] Sheu BC, Lien HC, Ho HN, Lin HH, Chow SN, Huang SC, Hsu SM. Increased expression and activation of ge-latinolytic matrix metalloproteinases is associated with the progression and recurrence of human cervical cancer. Cancer Res, 2003, 63(19): 6537-6542.[31] Zambon CF, Navaglia F, Basso D, Rugge M, Plebani M. Helicobacter pylori babA2, cagA, and s1 vacA genes work synergistically in causing intestinal metaplasia. J Clin Pathol, 2003, 56(4): 287-291.[32] Tsutsumi R, Takahashi A, Azuma T, Higashi H, Hatake-yama M. Focal adhesion kinase is a substrate and down-stream effector of SH.PYLORI-2 complexed with Helicobacter pylori CagA. Mol Cell Biol, 2006, 26(1): 261-276.[33] Mahdavi J, Sondén B, Hurtig M, Olfat FO, Forsberg L, Roche N, Ångström J, Larsson T, Teneberg S, Karlsson KA, Altraja S, Wadström T, Kersulyte D, Berg DE, Dubois A, Petersson C, Magnusson KE, Norberg T, Lindh F, Lundskog BB, Arnqvist A, Hammarström L, Borén T. Helicobacter pylori SabA adhesion in persistent infection and chronic inflammation. Science, 2002, 297(5581): 537-578.[34] Yanai A, Maeda S, Hikiba Y, Shibata W, Ohmae T, Hirata Y, Ogura K, Yoshida H, Omata M. Clinical relevance of Helicobacter pylori sabA genotype in Japanese clinical isolates. J Gastroenterol Hepatol, 2007, 22(12): 2228-2232.[35] Peek RM Jr, Thompson SA, Donahue JP, Tham KT, Atherton JC, Blaser MJ, Miller GG. Adherence to gastric epithelial cells induces expression of a Helicobacter pylori gene, iceA, that is associated with clinical outcome. Proc Assoc Am Physicians, 1998, 110(6): 531-544.[36] Nishiya D, Shimoyama T, Fukuda S, Yoshimura T, Tanaka M, Munakata A. Evaluation of the clinical relevance of the iceA1 gene in patients with Helicobacter pylori infection in Japan. Scand J Gastroenterol, 2000, 35(1): 36-39.[37] Yamaoka Y, Kodama T, Gutierrez O, Kim JG, Kashima K, Graham DY. Relationship between Helicobacter pylori iceA, cagA, and vacA status and clinical outcome: studies in four different countries. J Clin Microbiol, 1999, 37(7): 2274-2279.[38] Ashour AAR, Collares GB, Mendes EN, de Gusmão VR, de Magalhães Queiroz DM, Magalhães PP, de Carvalho AS, de Oliveira CA, Nogueira AMMF, Rocha GA, Rocha AMC. iceA genotypes of Helicobacter pylori strains isolated from Brazilian children and adults. J Clin Microbiol, 2001, 39(5): 1746-1750.[39] Dossumbekova A, Prinz C, Mages J, Lang R, Kusters JG, van Vliet AHM, Reindl W, Backert S, Saur D, Schmid RM, Rad RL. Helicobacter pylori HopH (OipA) and bacterial pathogenicity: genetic and functional genomic analysis of HopH gene polymorphisms. J Infect Dis, 2006, 194(10): 1346-1355.[40] Yamaoka Y, Ojo O, Fujimoto S, Odenbreit S, Haas R, Gutierrez O, El-Zimaity HMT, Reddy R, Arnqvist A, Graham DY. Helicobacter pylori outer membrane proteins and gastroduoedenal disease. Gut, 2006, 55(6): 775-781.[41] Israel DA, Salama N, Krishna U, Rieger UM, Atherton JC, Falkow S, Peek RM Jr. Helicobacter pylori genetic diversity within the gastric niche of a single human host. Proc Natl Acad Sci USA, 2001, 98(25): 14625-14630.[42] Kuipers EJ. Exploring the link between Helicobacter pylori and gastric cancer. Aliment Pharmacol Ther, 1999, 13(Suppl. 1): 3-11.[43] Occhialini A, Marais A, Alm R, Garcia F, Sierra R, Mégraud F. Distribution of open reading frames of plasticity region of reading frames of plasticity region of strain J99 in Helicobacter pylori strains isolated from gastric carcinoma and gastritis patients in Costa Rica. Infect Immun, 2000, 68(11): 6240-6249.[44] Santos A, Queiroz DMM, Ménard A, Marais A, Rocha GA, Oliveira CA, Nogueira AMF, Uzeda M, Mégraud F. New pathogenicity marker found in the Plasticity Region of the Helicobacter pylori genome. J Clin Microbiol, 2003, 41(4): 1651-1655.[45] de Jonge R, Kuipers EJ, Langeveld SCL, Loffeld RJLF, Stoof J, van Vliet AHM, Kusters JG. The Helicobacter pylori plasticity region locus jhp0947-jhp0949 is associated with duodenal ulcer disease and interleukin-12 production in monocyte cells. FEMS Immunol Med Microbiol, 2004, 41(2): 161-167.[46] Lu H, Hsu PI, Graham DY, Yamaoka Y. Duodenal ulcer promoting gene of Helicobacter pylori. Gastroenterology, 2005, 128(4): 833-844.[47] Gomes LI, Rocha GA, Rocha AMC, Soares TF, Oliveira CA, Bittencourt PFS, Queiroz DMM. Lack of association between Helicobacter pylori infection with dupA-positive strains and gastroduodenal diseases in Brazilian patients. Int J Med Microbiol, 2008, 298(3-4): 223-230.[48] Douraghi M, Mohammadi M, Oghalaie A, Abdirad A, Mohagheghi MA, Hosseini ME, Zeraati H, Ghasemi A, Esmaieli M, Mohajerani N. DupA as a risk determinant in Helicobacter pylori infection. J Med Microbiol, 2008, 57(pt 5): 554-562.[49] Argent RH, Burette A, Miendje Deyi VY, Atherton JC. The presence of dupA in Helicobacter pylori is not significantly associated with duodenal ulceration in Bel-gium, South Africa, China, or North America. Clin Infect Dis, 2007, 45(9): 1204-1206.[50] ElOmar EM. The importance of interleukin 1β in Helicobacter pylori associated disease. Gut, 2001, 48(6): 743-747.[51] Tu SP, Bhagat G, Cui GL, Takaishi S, Kurt-Jones EA, Rickman B, Betz KS, Penz-Oesterreicher M, Bjorkdahl O, Fox JG, Wang TC. Overexpression of interleukin-1β induces gastric in?ammation and cancer and mobilizes myeloid-derived suppressor cells in mice. Cancer Cell, 2008, 14(5): 408-419.[52] El-Omar EM, Carrington M, Chow WH, McColl KEL, Breamk JH, Youngk HA, Herrera J, Lissowska J, Yuan CC, Rothman N, Lanyon G, Martin M, Fraumeni JF Jr, Rabkin CS. Interleukin-1 polymorphisms associated with in-creased risk of gastric cancer. Nature, 2000, 404(6776): 398-402.[53] 何彩云, 袁媛. 宿主基因单核苷酸多态性与幽门螺杆菌相关胃癌. 遗传, 2011, 33(2): 109-116[54] El-Omar EM, Rabkin CS, Gammon MD, Vaughan TL, Risch HA, Schoenberg JB, Stanford JL, Mayne ST, Goedert J, Blot WJ, Fraumeni JF Jr, Chow WH. Increased risk of Noncardia gastric cancer asociated with proinflammatory cytokine gene polymorphisms. Gastroenterology, 2003, 124(5): 1193-1201.[55] Arbour NC, Lorenz E, Schutte BC, Zabner J, Kline JN, Jones M, Frees K, Watt JL, Schwartz DA. TLR4 mutations are associated with endotoxin hyporesponsiveness in humans. Nat Genet, 2000, 25(2): 187-191.[56] Franchimont D, Vermeire S, El Housni H, Pierik M, van Steen K, Gustot T, Quertinmont E, Abramowicz M, van Gossum A, Devière J, Rutgeerts P. De?cient host-bacteria interactions in in?ammatory bowel disease? The toll-like receptor (TLR)-4 Asp299gly polymorphism is associated with Crohn’s disease and ulcerative colitis. Gut, 2004, 53(7): 987-992.[57] Lorenz E, Mira JP, Frees KL, Schwartz DA. Relevance of mutations in the TLR4 receptor in patients with gram-negative septic shock. Arch Intern Med, 2002, 162(9): 1028-1032.[58] Kiechl S, Lorenz E, Reindl M, Wiedermann CJ, Oberhol-lenzer F, Bonora E, Willeit J, Schwartz DA. Toll-like receptor 4 polymorphisms and atherogenesis. N Engl J Med, 2002, 347(3): 185-192.[59] Hold GL, Rabkin CS, Chow WH, Smith MG, Gammon MD, Risch HA, Vaughan TL, McColl KE, Lissowska J, Zatonski W, Schoenberg JB, Blot WJ, Mowat NAG, Fraumeni JF Jr, El-Omar EM. A functional polymorphism of toll-like receptor 4 gene increases risk of gastric carcinoma and its precursors. Gastroenterology, 2007, 132(3): 905-912.[60] Tahara T, Arisawa T, Wang FY, Shibata T, Nakamura M, Sakata M, Hirata I, Nakano H. Toll-like receptor 2-196 to 174del polymorphism influences the susceptibility of Japanese people to gastric cancer. Cancer Sci, 2007, 98(11): 1790-1794.[61] Ng MTH, Van't Hof R, Crockett JC, Hope ME, Berry S, Thomson J, McLean MH, McColl KEL, El-Omar EM, Hold GL. Increase in NF-кB binding affinity of the C allelic variant of the Toll-like receptor 9 -1237T/C polymorphism is associated with Helicobacter pylori induced gastric disease. Infect Immun, 2010, 78(3): 1345-1352.[62] 李昭辉, 王占民, 张联, 潘凯枫, 张春凤, 宁涛, 柯杨. 山东临朐人群HLA等位基因多态性与幽门螺杆菌感染关系的研究. 遗传, 2004, 26(2): 143-146.[63] Azuma T, Ito S, Sato F, Yamazaki Y, Miyaji H, Ito Y, Suto H, Kuriyama M, Kato T, Kohli Y. The role of the HLA-DQA1 gene in resistance to atrophic gastritis and gastric adenocarcinoma induced by Helicobacter pylori infection. Cancer, 1998, 82(6): 1013-1018.[64] Magnusson PKE, Enroth H, Eriksson I, Held M, Nyrén O, Engstrand L, Hansson LE, Gyllensten UB. Gastric cancer and human leukocyte antigen: distinct DQ and DR alleles are associated with development of gastric cancer and infection by Helicobacter pylori. Cancer Res, 2001, 61(6): 2684-2689.[65] Bond GL, Hu WW, Bond EE, Robins H, Lutzker SG, Arva NC, Bargonetti J, Bartel F, Taubert H, Wuerl P, Onel K, Yip L, Hwang SJ, Strong LC, Lozano G, Levine AJ. A sin-gle nucleotide polymorphism in the MDM2 promoter attenuates the p53 tumor suppressor pathway and acceler-ates tumor formation in humans. Cell, 2004, 119(5): 591-602.[66] Wang XY, Yang Y, Ho B, Yang Y, Huang ZH, Zhang ZH, Zhang GX. Interaction of Helicobacter pylori with genetic variants in the MDM2 promoter, is associated with gastric cancer susceptibility in Chinese patients. Helicobacter, 2009, 14(5): 466-471.[67] Sun LP, Guo XL, Zhang Y, Chen W, Bai XL, Liu J, Yuan Y. Impact of pepsinogen C polymorphism on individual susceptibility to gastric cancer and its precancerous conditions in a Northeast Chinese population. J Cancer Res Clin Oncol, 2009, 135(8): 1033-1039. |
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