期刊论文详细信息
BMC Microbiology
Comparison of the major virulence-related genes of Listeria monocytogenes in Internalin A truncated strain 36-25-1 and a clinical wild-type strain
Bon Kimura1  Takashi Kuda1  Satoko Miya1  Hajime Takahashi1  Daisuke Kyoui1 
[1] Department of Food Science and Technology, Faculty of Marine Science, Tokyo University of Marine Science and Technology, 4-5-7 Konan, Minato, Tokyo 108-8477, Japan
关键词: Next-generation-sequencing;    Internalin A;    Listeria monocytogenes;   
Others  :  1142100
DOI  :  10.1186/1471-2180-14-15
 received in 2013-09-04, accepted in 2014-01-21,  发布年份 2014
PDF
【 摘 要 】

Background

Internalin A (InlA) facilitates the invasion of Listeria monocytogenes into a host cell. Some strains of Listeria monocytogenes express truncated forms of InlA, which reduces invasiveness. However, few virulence-related genes other than inlA have been analyzed in InlA-truncated strains. In the present study, we sequenced the draft genome of strain 36-25-1, an InlA-truncated strain, with pyrosequencing and compared 36 major virulence-related genes in this strain and a clinical wild-type strain.

Results

Strain 36-25-1 possessed all of the virulence-related genes analyzed. Of the analyzed genes, only 4 genes (dltA, gtcA, iap, and inlA) differed when the nucleotide sequences of strain 36-25-1 and the clinical wild-type strain were compared. Analysis of the deduced amino acid sequences found no mutations that significantly influenced virulence in genes other than inlA.

Conclusions

The virulence-associated genes in strain 36-25-1 differ little from those of the clinical wild-type strain, indicating that a slight mutation in the nucleotide sequence determines the virulence of the InlA-truncated strain. In addition, the results suggest that, aside from InlA-mediated cell invasiveness, there is almost no difference between the virulence of strain 36-25-1 and that of the clinical wild-type strain.

【 授权许可】

   
2014 Kyoui et al.; licensee BioMed Central Ltd.

【 预 览 】
附件列表
Files Size Format View
20150327215305848.pdf 556KB PDF download
Figure 1. 121KB Image download
【 图 表 】

Figure 1.

【 参考文献 】
  • [1]Swaminathan B, Gerner-Smidt P: The epidemiology of human listeriosis. Microbes Infect 2007, 9:1236-1243.
  • [2]Ivanek R, Gröhn YT, Wiedmann M: Listeria monocytogenes in multiple habitats and host populations: review of available data for mathematical modeling. Foodborne Pathog Dis 2006, 3:4.
  • [3]Rocourt J, BenEmbarek P, Toyofuku H, Schlundt J: Quantitative risk assessment of Listeria monocytogenes in ready-to-eat foods: the FAO/WHO approach. FEMS Immunol Med Microbiol 2003, 33:263-267.
  • [4]U.S. Department of Health and Human Service, U.S. Department of Agriculture Food Safety and Inspection service, and Centers for Disease Control: Quantitative assessment of the relative risk to public health from foodborne Listeria monocytogenes among selected categories of ready-to-eat foods. Washington, D.C: United States Department of Health and Human Services and United States Department of Agriculture; 2003. http://www.fda.gov/Food/FoodScienceResearch/RiskSafetyAssessment/ucm183966.htm webcite
  • [5]World Health Organization, Food and Agriculture Organization of the United Nations: Risk assessment of Listeria monocytogenes in ready-to-eat foods. Microbiological risk assessment series 5. Roma, Italy: Food and Agriculture Organization of the United Nations and World Health Organization; 2004. http://www.fao.org/docrep/010/y5394e/y5394e00.HTM webcite
  • [6]Gaillard JL, Berche P, Frehel C, Gouin E, Cossart P: Entry of L. monocytogenes into cells is mediated by internalin, a repeat protein reminiscent of surface antigens from gram-positive cocci. Cell 1991, 65:1127-1141.
  • [7]Mengaud J, Ohayon H, Gounon P, Mège RM, Cossart P: E-cadherin is the receptor for internalin, a surface protein required for entry of L. monocytogenes into epithelial cells. Cell 1996, 84:923-932.
  • [8]Miya S, Takahashi H, Ishikawa T, Fujii T, Kimura B: Risk of Listeria monocytogenes contamination of raw ready-tp-eat seafood products available at retail outlets in Japan. Appl Environ Microbiol 2010, 76:3383-3386.
  • [9]Schubert WD, Urbanke C, Ziehm T, Beier V, Machner MP, Domann E, Wehland J, Chakraborty T, Heinz DW: Structure of internalin, a major invasion protein of Listeria monocytogenes, in complex with its human receptor E-cadherin. Cell 2002, 111:825-836.
  • [10]Chen Y, Ross WH, Whiting RC, Van Stelten A, Nightingale KK, Wiedmann M, Scott VN: Variation in Listeria monocytogenes dose responses in relation to subtypes encoding a full-length or truncated internalin A. Appl Environ Microbiol 2011, 77:4.
  • [11]Handa-Miya S, Kimura B, Takahashi H, Sato M, Ishikawa T, Igarashi K, Fujii T: Nonsense-mutated inlA and prfA not widely distributed in Listeria monocytogenes isolates from ready-to-eat seafood products in Japan. Int J Food Microbiol 2007, 117:312-318.
  • [12]Jonquières R, Bierne H, Mengaud J, Cossart P: The inlA gene of Listeria monocytogenes LO28 harbors a nonsense mutation resulting in release of internalin. Infect Immun 1998, 66:7.
  • [13]Olier M, Garmyn D, Rousseaux S, Lemaître JP, Piveteau P, Guzzo J: Truncated internalin A and asymptomatic Listeria monocytogenes carriage: in vivo investigation by allelic exchange. Infect Immun 2005, 73:644-648.
  • [14]Van Stelten A, Simpson JM, Chen Y, Scott VN, Whiting RC, Ross WH, Nightingale KK: Significant shift in median guinea pig infectious dose shown by an outbreak-associated Listeria monocytogenes epidemic clone strain and a strain carrying a premature stop codon mutation in inlA. Appl Environ Microbiol 2011, 77:2479-2487.
  • [15]Jacquet C, Doumith M, Gordon JI, Martin PMV, Cossart P, Lecuit M: A molecular marker for evaluating the pathogenic potential of foodborne Listeria monocytogenes. J Infect Dis 2004, 189:2094-2100.
  • [16]Van Stelten A, Simpson JM, Ward TJ, Nightingale KK: Revelation by single-nucleotide polymorphism genotyping that mutations leading to a premature stop codon in inlA are common among Listeria monocytogenes isolates from ready-to-eat foods but not human listeriosis cases. Appl Environ Microbiol 2010, 76:2783-2790.
  • [17]Témoin S, Roche SM, Grépinet O, Fardini Y, Velge P: Multiple point mutations in virulence genes explain the low virulence of Listeria monocytogenes field strains. Microbiol 2008, 154:939-948.
  • [18]Camejo A, Carvalho F, Reis O, Leitão E, Sousa S, Cabanes D: The arsenal of virulence factors deployed by Listeria monocytogenes to promote its cell infection cycle. Virulence 2011, 2:379-394.
  • [19]Bakker HC, Cummings CA, Ferreira V, Vatta P, Orsi RH, Degoricija L, Barker M, Petrauskene O, Furtado MR, Wiedmann M: Comparative genomics of the bacterial genus Listeria: genome evolution is characterized by limited gene acquisition and limited gene loss. BMC Genomics 2010, 11:688. BioMed Central Full Text
  • [20]Hain T, Ghai R, Billion A, Kuenne CT, Steinweg C, Izar B, Mohamed W, Mraheil MA, Domann E, Schaffrath S, Kärst U, Goesmann A, Oehm S, Pühler A, Merkl R, Vorwerk S, Glaser P, Garrido P, Rusniok C, Buchrieser C, Goebel W, Chakraborty T: Comparative genomics and transcriptomics of lineages I, II, and III strains of Listeria monocytogenes. BMC Genomics 2012, 13:144. BioMed Central Full Text
  • [21]Bierne H, Cossart P: Listeria monocytogenes surface proteins: from genome predictions to function. Microbiol Mol Biol Rev 2007, 71:377-397.
  • [22]Abachin E, Poyart C, Pellegrini E, Milohanic E, Fiedler F, Berche P, Trieu-Cuot P: Formation of D-alanyl-lipoteichoic acid is required for adhesion and virulence of Listeria monocytogenes. Mol Microbiol 2002, 43:1-14.
  • [23]Bubert A, Kuhn M, Goebel W, Köhler S: Structural and functional properties of the p60 proteins from different Listeria species. J Bacteriol 1992, 174:8166-8171.
  • [24]Pilgrim S, Kolb-Mäurer A, Gentschev I, Goebel W, Kuhn M: Deletion of the gene encoding p60 in Listeria monocytogenes leads to abnormal cell division and loss of actin-based motility. Infect Immun 2003, 71:3473-3484.
  • [25]Rasmussen OF, Skouboe P, Dons L, Rossen L, Olsen JE: Listeria monocytogenes exists in at least three evolutionary lines: evidence from flagellin, invasive associated protein and listeriolysin O genes. Microbiol 1995, 141:2053-2061.
  • [26]Schmid M, Walcher M, Bubert A, Wagner M, Wagner M, Schleifer KH: Nucleic acid-based, cultivation-independent detection of Listeria spp. and genotypes of L. monocytogenes. FEMS Immunol Med Microbiol 2003, 35:215-225.
  • [27]Cabanes D, Dehoux P, Dussurget O, Frangeul L, Cossart P: Surface proteins and the pathogenic potential of Listeria monocytogenes. Trends Microbiol 2002, 10:5.
  • [28]Köhler S, Leimeister-Wächter M, Chakraborty T, Lottspeich F, Goebel W: The gene coding for protein p60 of Listeria monocytogenes and its use as a specific probe for Listeria monocytogenes. Infect Immun 1990, 58:1943-1950.
  • [29]Takahashi H, Handa-Miya S, Kimura B, Sato M, Yokoi A, Goto S, Watanabe I, Koda T, Hisa K, Fujii T: Development of multilocus single strand conformation polymorphism (MLSSCP) analysis of virulence genes of Listeria monocytogenes and comparison with existing DNA typing methods. Int J Food Microbiol 2007, 118:274-284.
  • [30]Sambrook J, Fritsch EF, Maniatis T: Molecular cloning: a laboratory manual. 2nd edition. Cold Spring HarborCold: Spring Harbor Laboratory Press; 1989.
  文献评价指标  
  下载次数:7次 浏览次数:13次