S100A8 and infection: Thus, in AGS cells we see a reduction in CagA translocation to approximately 50% when a HopQ-deficient versus a wild type Hp strain is used for infection (Fig 3A) [19], which is in contrast to KatoIII cells suggesting that in AGS gastric epithelial cells an additional, so far unknown receptor might be expressed, which is probably targeted by another Hp adhesin to support CagA translocation.