The Bronze Age of science in Spain.

in conjunction with our results, demonstrate that in certain H. pylori strains, CagA plays an essential role in the activation of NF-κB. We acknowledge in our article that CagA may not be the only component that H. pylori uses to activate inflammation. Compelling evidence exists that under some circumstances other H. pylori factors can induce an inflammatory response. For example, CagA clearly does not seem to be essential for activation of NF-κB in HEK293 cells or macrophages (Maeda et al, 2001; Viala et al, 2004). Previous studies have also convincingly demonstrated that among populations of H. pylori cagApositive strains, the ability of CagA to activate NF-κB is strain-specific (Brandt et al, 2005). Thus, the accompanying remarks from Schweitzer et al underscore the importance of considering the experimental model when studying H. pylori-mediated inflammation. The goal of our work was to decipher the molecular mechanism for the activation of NF-κB by H. pylori. In that context, our study provides new insight into the pathogen-effector-induced activation of the inflammatory response.