Abstract

We refer to the publication by Lamb et al (2009). This report describes the Helicobacter pylori virulence factor cytotoxin‐associated gene A (CagA), encoded in the pathogenicity island (PAI), as essential for the rapid activation of the transcription factor nuclear factor κB (NF‐κB) in epithelial cells. The authors reported fast NF‐κB activation in AGS (human gastric carcinoma) cells infected with H. pylori G27 wild type, but not with the isogenic CagA‐deficient strain, determined by IκBα phosphorylation and degradation, RelA phosphorylation, NF‐κB DNA‐binding, and interleukin 8 (IL‐8) mRNA expression. However, the profound CagA dependency of NF‐κB activation, representing the centrepiece of the study by Lamb et al (2009), is in clear contradiction to previously …

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