TABLE 2.

Responses of 19 mammalian cell lines to infection with H. pylori strain P1

Cell typeCell lineOrganismTissueCagA phosphory- lationaCagA pro- cessingHost cell protein dephosphory- lationCellular phenotypeIL-8 secretionb
Human gastric cellsAGSHumanStomach++++Hummingbird (CagA dependent)+
MKN-45HumanStomach++++++
MKN-28HumanStomach+++
Kato 3HumanStomach+++++
Human nongastric cellsHT29HumanColon++++
HeLaHumanCervix+++
GLC4HumanLung
Hec1.bHumanEndometrium+++
293THumanKidney++++
HLHumanLung+++
THP1HumanBlood++Homotypic aggregation (TFSS+
HepG2HumanLiver+++    dependent)+
Nonhuman nongastricCHO K1HamsterOvaryND
    cellsCos-1African green monkeyKidney+ND
J774.AMouseBlood++++(Mip-2)
MDCKDogKidneyND
SR 4987MouseBone marrow+− (Mip-2)
SYF+srcMouseConnective tissue+− (Mip-2)
L929MouseConnective tissue+− (Mip-2)
  • a Intensity of CagA-tyrosine phosphorylation relative to that in AGS cells (see Fig. 1A for further details).

  • b At least a twofold increase in IL-8 secretion compared to that by P1ΔvirB11 is indicated by “+”(see Fig. 2). With the mouse cell lines, we analyzed the secretion of the murine IL-8 analog Mip-2, as indicated. Proinflammatory responses in CHO K1, Cos-1, and MDCK cells could not be determined (ND). For details, see Materials and Methods.