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. 2002 Feb;70(2):665–671. doi: 10.1128/iai.70.2.665-671.2002

TABLE 1.

Translocation and tyrosine phosphorylation of CagA, induction of the scattering phenotype, and secretion of IL-8 in AGS cells infected with H. pyloria

Bacterial strain Mutated ORFb CagA expres- sion CagA trans- location/phos- phorylation Induction of scattering phenotype Induction of IL-8 secretion
P1 wt + + + +
P12 wt + + + +
G27 wt + + + +
J99 wt + +
P12ΔvacA HP0887 + + + +
P1ΔalpA/B HP0912/HP0913 +
P12Δcag PA1 HP520-HP547
P1ΔvirB4 HP0544 +
P1ΔvirB7 HP0532 +
P1ΔvirB8 HP0529 +
P1ΔvirB9 HP0528 +
P1ΔvirB10 HP0527 +
P1ΔvirB11 HP0525 +
P1ΔvirD4 HP0524 + +
P1ΔcagA HP0547 +
G27ΔcagF HP0543 +
P1ΔcagH HP0541 +
G27ΔcagI HP0540 +
G27ΔcagM HP0537 +
P1ΔcagA/cagA HP0547 + + + +
P1ΔvirD4/virD4 HP0524 + + + +
a

All H. pylori strains are type I isolates. cag PA1 mutagenesis and genetic complementation are described in Materials and Methods (see also Fig. 1). Bacterial infection was for 6h at an MOI of 100. CagA translation and tyrosine phosphorylation were detected by immunoblot analysis. IL-8 production was determined by ELISA. wt, wild type

b

From Tomb et al. (39).