The vacuolating toxin of Helicobacter pylori mimicks the CFTR-mediated chloride conductance.

Cystic fibrosis (CF) is caused by defects of the CF transmembrane conductance regulator (CFTR), which acts both as an anion-selective channel and as a regulator of other proteins. The relative contribution of these two functions in CF disease is debated. The toxin VacA forms channels with properties similar to those of the CFTR, and we report here that it can insert into the membrane of various cells originating from respiratory epithelia, generating a chloride conductance comparable to that produced by activation of the CFTR. VacA may therefore become a valuable tool in the study of CF pathogenesis.