Modulation of host cell signal transduction pathways by Helicobacter pylori infection

被引:4
作者
Ceponis, PJM
Jones, NL
机构
[1] Hosp Sick Children, Res Inst, Toronto, ON M5G 1X8, Canada
[2] Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada
[3] Univ Toronto, Dept Paediat, Toronto, ON, Canada
关键词
epithelium; H pylori; signal transduction;
D O I
10.1155/2005/731817
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Bacterial pathogens modulate host cell signal transduction responses to establish infection and cause disease. The purpose of the present summary, first presented at the Canadian Helicobacter Study Group meeting, is to discuss current knowledge of specific Helicobacter pylori factors, including the vacuolating cytotoxin, cytotoxin-associated gene A and the type four secretion system encoded by the cytotoxin-associated gene pathogenicity island and review the host cell signal transduction cascades that they modulate.
引用
收藏
页码:415 / 420
页数:6
相关论文
共 88 条
  • [31] HELICOBACTER-MUSTELAE AND HELICOBACTER-PYLORI BIND TO COMMON LIPID RECEPTORS INVITRO
    GOLD, BD
    HUESCA, M
    SHERMAN, PM
    LINGWOOD, CA
    [J]. INFECTION AND IMMUNITY, 1993, 61 (06) : 2632 - 2638
  • [32] Cag pathogenicity island-specific responses of gastric epithelial cells to Helicobacter pylori infection
    Guillemin, K
    Salama, NR
    Tompkins, LS
    Falkow, S
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (23) : 15136 - 15141
  • [33] Proteomic analysis of the intestinal epithelial cell response to enteropathogenic Escherichia coli
    Hardwidge, PR
    Rodriguez-Escudero, I
    Goode, D
    Donohoe, S
    Eng, J
    Goodlett, DR
    Aebersold, R
    Finlay, BB
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (19) : 20127 - 20136
  • [34] Helicobacter pylori and two ultrastructurally distinct layers of gastric mucous cell mucins in the surface mucous gel layer
    Hidaka, E
    Ota, H
    Hidaka, H
    Hayama, M
    Matsuzawa, K
    Akamatsu, T
    Nakayama, J
    Katsuyama, T
    [J]. GUT, 2001, 49 (04) : 474 - 480
  • [35] Biological activity of the Helicobacter pylori virulence factor CagA is determined by variation in the tyrosine phosphorylation sites
    Higashi, H
    Tsutsumi, R
    Fujita, A
    Yamazaki, S
    Asaka, M
    Azuma, T
    Hatakeyama, M
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (22) : 14428 - 14433
  • [36] SHP-2 tyrosine phosphatase as an intracellular target of Helicobacter pylori CagA protein
    Higashi, H
    Tsutsumi, R
    Muto, S
    Sugiyama, T
    Azuma, T
    Asaka, M
    Hatakeyama, M
    [J]. SCIENCE, 2002, 295 (5555) : 683 - 686
  • [37] HIRAI M, 1994, INT J CANCER, V56, P56, DOI 10.1002/ijc.2910560111
  • [38] Inhibition of stress-activated MAP kinases induces clinical improvement in moderate to severe Crohn's disease
    Hommes, D
    Van Den Blink, B
    Plasse, T
    Bartelsman, J
    Xu, CP
    MacPherson, B
    Tytgat, G
    Peppelenbosch, M
    Van Deventer, S
    [J]. GASTROENTEROLOGY, 2002, 122 (01) : 7 - 14
  • [39] Meta-analysis of the relationship between cagA seropositivity and gastric cancer
    Huang, JQ
    Zheng, GF
    Sumanac, K
    Irvine, EJ
    Hunt, RH
    [J]. GASTROENTEROLOGY, 2003, 125 (06) : 1636 - 1644
  • [40] Acidic pH changes receptor binding specificity of Helicobacter pylori: A binary adhesion model in which surface heat shock (stress) proteins mediate sulfatide recognition in gastric colonization
    Huesca, M
    Borgia, S
    Hoffman, P
    Lingwood, CA
    [J]. INFECTION AND IMMUNITY, 1996, 64 (07) : 2643 - 2648