期刊文献+

艰难梭菌引起抗感染免疫的主要致病因子及其基因功能的研究进展 被引量:4

Clostridium difficile virulence factors inducing anti-infection response and its gene functions
下载PDF
导出
摘要 艰难梭菌是医院感染性腹泻中最常见的病原菌之一,在过去10年中,由于ribotyping 027型等高毒菌株的出现,全球艰难梭菌感染相关性疾病发病率显著上升,已经成为欧美许多国家法定传染病必报的监测病原。致病艰难梭菌的毒力因子主要包括A毒素和B毒素,刺激机体发生免疫应答。除外A、B毒素,少数艰难梭菌还产生二元毒素。本文对近年来艰难梭菌引起机体抗感染免疫的相关致病因子及其基因功能的最新研究进展进行了回顾和总结,并重点探讨了主要致病因子A毒素和B毒素结构功能及基因表达调控特征,包括构建A、B毒素分子模型,致病基因编码区多态性特征,以及负向调控因子tcdC的变异及影响,对未来疫苗靶位点的筛选以及艰难梭菌致病机制中信号转导研究具有指导意义。 Clostridium difficile is one of the most common causes for hospital acquired diarrhea. During the past decade, incidence of Clostridium difficile associated disease has significantly increased worldwide coincident with emerging of hypervirulent strain ribotyping 027, and this microorganism has been included into monitoring pathogens of national notable disease in several western countries. Hosts immune responses to virulence factors, mainly toxin A and toxin B produced by toxigenic strains, directly influence the development of disease. Further more, a number of strains express an additional toxin termed binary toxin. In this paper, we retrospect and summarize the latest advancement of the gene functions of Clostridium difficile virulence factors inducing anti- infection response, and primarily discuss the characteristics of molecular model and gene regulation of toxin A and toxin B, which will be a basis for study on screen of possible vaccine antigen target and signal transduction in pathogenic mechanism of Clostridium diifficile.
出处 《免疫学杂志》 CAS CSCD 北大核心 2013年第4期357-360,共4页 Immunological Journal
基金 国家自然科学基金青年基金(81101218) 中国疾病预防控制中心青年基金(2011A101)
关键词 艰难梭菌 抗感染免疫 A毒素 B毒素 tcdA tcdB 二元毒素 Clostridium diffiicle Anti-infection immunity Toxin A/Toxin B tcdA/tcdB Binary toxin
  • 相关文献

参考文献25

  • 1Rupnik M, Wilcox MH, Gerding DN. Clostridium difficile infection: new developments in epidemiology and pathogenesis [J]. Nat Rev Microbiol, 2009, 7(7): 526-536.
  • 2Gravel D, Miller M, Simor A, et al. Health care-associated Clostridium difficile infection in adults admitted to acute care hospitals in Canada: a Canadian Nosocomial Infection Surveillance Program Study[J]. Clin Infect Dis, 2009, 48(5): 568-576.
  • 3Bauer MP, Notermans DW, Van Benthem BH, et al. Clostridium difficile infection in Europe: a hospital-based survey[J]. Lancet, 2011, 377(9759): 63-73.
  • 4Jank T, Aktories K. Structure and mode of action of clostridial glucosylating toxins: the ABCD model[J]. Trends Microbiol, 2008, 16(5): 222-229.
  • 5Pruitt RN, Chambers MG, Ng KK, et al. Structural organization of the functional domains of Clostridium difficile toxins A and B[J]. Proc Natl Acad Sci USA, 2010, 107(30): 13467-13472.
  • 6Permpoonpattana P, Hong HA, Phetcharaburanin J, et al. Immunization with Bacillus spores expressing toxin A peptide repeats protects against infection with Clostridium difficile strains producing toxins A and B[J]. Infect Immun, 2011, 79(6): 2295-2302.
  • 7Lyras D, O'Connor JR, Howarth PM, et al. Toxin B is essential for virulence of Clostridium difficile [J]. Nature, 2009, 458(7242): 1176-1179.
  • 8Kuehne SA, Cartman ST, Heap JT, et al. The role of toxin A and toxin B in Clostridium difficile infection[J]. Nature, 2010, 467(7316): 711-713.
  • 9White R, Chiba S, Pang T, et al. Holin triggering in real time[J]. Proc Natl Acad Sci USA, 2011, 108(2): 798-803.
  • 10Govind R, Dupuy B. Secretion of Clostridium difficile toxins A and B requires the Holin-like protein TcdE [J].PLoS Pathog, 2012, 8(6): e1002727.

二级参考文献12

  • 1Lowy FD. Staphylococcus aureus infections[J]. N Engl J Med,1998, 339(8): 520-532.
  • 2Fowler VG, Miro JM, Hoen B,et al. Staphylococcus aureusendocarditis: a consequence of medical progress[J]. JAMA,2005,293(24): 3012-3021.
  • 3Hiramatsu K. Vancomycin-resistant Staphylococcus aureus:a new model of antibiotic resistance[J]. Lancet Infect Dis,2001, 1(3): 147-155.
  • 4Arrecubieta C,Matsunaga I,Asai T, et al. Vaccination withclumping factor A and fibronectin binding protein A toprevent Staphylococcus aureus infection of an aortic patchin mice[J]. J Infect Dis, 2008,198(4): 571-575.
  • 5DeDent A,Kim HK, Missiakas D, et al, Exploringstaphylococcus aureus pathways to disease for vaccinedevelopment[J]. Semin Immunopathol, 2012, 34(2): 317-333.
  • 6Bubeck WJ, Schneewind 0. Vaccine protection againstStaphylococcus aureus pneumonia|J|. J Exp Med, 2008,205(2):287-294.
  • 7Kuklin NA, Clark DJ, Secore S, et al. A novelStaphylococcus aureus vaccine: iron surface determinant Binduces rapid antibody responses in rhesus macaques andspecific increased survival in a murine S. aureus sepsismodelfj]. Infect Immun, 2006,74(4): 2215-2223.
  • 8Hu C,Gong R,Guo A,et al. Protective effect of ligand -binding domain of fibronectin -binding protein on mastitisinduced by Staphylococcus aureus in mice [J] Vaccine, 2010,28(24): 4038-4044.
  • 9Joshi A, Pancari G,Cope L, et al. Immunization withStaphylococcus aureus iron regulated surface determinantB (IsdB) confers protection via Thl7/IL17 pathway in amurine sepsis model 见 Hum Vaccin Immunother, 2012, 8(3):336-346.
  • 10Lin L, Ibrahim AS, Xu X, et al. Thl -Thl7 cells mediateprotective adaptive immunity against Staphyiococcus aureusand Candida albicans infection in mice[J]. PLoS Pathog,2009,5(12): e 1000703.

共引文献6

同被引文献51

  • 1Freeman J,Bauer MP, Baines SD, et al. The changing epidemi- ology of Clostridium difficile infections [ J]. Clin Microbiol Rev, 2010.23 ( 3 ) :529 - 549.
  • 2Lyras D, O'Connor JR, Howarth PM,et al. Toxin B is essential for virulence of Clostridium difficile [ J ]. Nature, 2009, 458 (7242) :1176 - 1179.
  • 3Goldenberg SD, Cliff PR, French GL,et al. Glutamate dehydro- genase for laboratory, diagnosis of Clostridium difficile infection [J]. J Clin Microbiol,2010,48(8) :3050 -3051.
  • 4Pepin J, Saheb N, Coulombe MA, et al. Emergence of fluoroquin- olones as the predominant risk factor for Clostridium difficile asso- ciated diarrhea: a cohort study during an epidemic in Quebec [ J]. Clin Infect Dis,2005,41 (9) : 1254 - 1260.
  • 5Lemee L, Dhalluin A,Testelin S,et al. Multiplex PCR targeting tpi ( triose phosphate isomerase ), tcdA ( Toxin A ), and tcdB (Toxin B ) genes for toxigenic culture of Clostridiurn difficile[ J]. J Clin Microbio1,2004,42 ( 12 ) :5710 - 5714.
  • 6Wren MWD, Sivapalan M, Kinson R, et al. Laboratory diagnosis of Clostridium difficile infection. An evaluation of tests for fecal toxin,glutamate dehydrogenase, lactoferrin and toxigenic culture in the diagnostic laboratory[J]. Br J Biomed Sci,2009,66(1) :1-5.
  • 7Ananthakrishnan AN. Clostridium difltcile infection:epidemiolo- gy,risk factors and management[ J ]. Nat Rev Gastroenterol Hep- atol,2011,8( 1 ) :17 -26.
  • 8Ticehurst JR, Aird DZ, Dam LM, et al. Effective detection of toxi- genic Clostridium difficile by a two-step algorithm including tests for antigen and cytotoxin [ J ]. J Clin Microbiol, 2006,44 ( 3 ) : 1145 - 1149.
  • 9Hall IC, O' Toole E. Intestinal flora in new-born infants with a description of a new pathogenic anaerobe, Bacillus difficile [ J ]. Am J Dis Child,1935, 49(2) : 390 -402.
  • 10Curry SR, Marsh JW, Muto CA, et al. TcdC genotypes associat- ed with severe TcdC truncation in an epidemic clone and other strains of Clostridium diffwile [ J ]. J Clin Microhiol, 2007, 45 (1) :215 -221.

引证文献4

二级引证文献5

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部