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. 2005 Aug;73(8):4643–4652. doi: 10.1128/IAI.73.8.4643-4652.2005

TABLE 2.

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

Cell type Cell line Organism Tissue CagA phosphory- lationa CagA pro- cessing Host cell protein dephosphory- lation Cellular phenotype IL-8 secretionb
Human gastric cells AGS Human Stomach +++ + Hummingbird (CagA dependent) +
MKN-45 Human Stomach +++ + + +
MKN-28 Human Stomach ++ +
Kato 3 Human Stomach +++ + +
Human nongastric cells HT29 Human Colon ++ + +
HeLa Human Cervix ++ +
GLC4 Human Lung
Hec1.b Human Endometrium + + +
293T Human Kidney ++ + +
HL Human Lung ++ +
THP1 Human Blood + + Homotypic aggregation (TFSS +
HepG2 Human Liver ++ +     dependent) +
Nonhuman nongastric CHO K1 Hamster Ovary ND
    cells Cos-1 African green monkey Kidney + ND
J774.A Mouse Blood ++ + +(Mip-2)
MDCK Dog Kidney ND
SR 4987 Mouse Bone marrow + − (Mip-2)
SYF+src Mouse Connective tissue + − (Mip-2)
L929 Mouse Connective 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.