Table 1 Overview of H. pylori factors that interfere with host cell functions

Adhesins:

  BabA

Lewis B [14]; Lewis A [15]; Globo H hexaglycosylceramide [16]

Adhesion to host cells [14–16]

  SabA

Sialyl Lewis X, sialyl Lewis A [25]

Adhesion to host cells [25], elevated binding via induction of β3GnT5 [26]

  AlpA/B

Collagen IV, laminin [35, 37]

Adhesion to ECM [35, 37], reinforces NF-кB and MAPK signaling [33]

  OipA

Not known

Adhesion to host cells [38–40], induction of inflammatory response [38, 39]

  HopZ

Not known

Adhesion?

  HorB

Not known

Adhesion?

Secreted factors:

  Urease

Not known

Survival under acidic pH [66, 70], disruption of tight junctions [72, 75]

  VacA

EGFR [89, 90], RPTPα [91], RPTPβ [92], sphingomyelin [93], LRP1 [95]

Vacuolization [77, 78], apoptosis [98, 99], disruption of tight junctions [74]

  HtrA

E-cadherin [104]

Disruption of adherence junctions [104]

  GGT

Not known

Apoptosis [63], cell cycle arrest [64]

T4SS components:

  CagL

β₁-Integrin [119, 120]; (β₃) β₅-Integrin [122]

Facilitates CagA translocation [120]; activation of host kinases [120, 122]

  CagI

β₁-Integrin [119, 123]

Not known, necessary for CagA translocation and IL-8 induction [118, 123]

  CagY

β₁-Integrin [119]

Not known, necessary for CagA translocation and IL-8 induction [118]

  CagA

β₁-Integrin [119]

Not known (for intracellular actions see below)

Injected factors:

  CagA

c-Met, p120, E-cadherin, Grb-2, Par proteins, PLC-γ, TAK, ZO-1, etc. [143]

Disruption of junctions and polarity, inflammation, proliferation [143]

  Phospho-CagA

Src; SHP-2, Csk; c-Abl; Crk proteins, Grb2, Grb7, PI3K, Ras-GAP, SHP-1, etc. [143]

Cell elongation and cell motility [132, 133, 143], cancer development [146]

  Peptidoglycan

Nod1 [113, 152]

NF-κB activation [113]; AP-1 and MAPK activation [152]