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.
Campello
Silvia
S
CNR Institute of Neuroscience, Section for Biomembranes, University of Padova, Viale G. Colombo 3, 35121 Padua, Italy.
Tombola
Francesco
F
Cabrini
Giulio
G
Zoratti
Mario
M
D001426:Bacterial Proteins / Q000494:pharmacology*; D002460:Cell Line; D002478:Cells, Cultured; D002712:Chlorides / Q000378:metabolism*; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000502:physiology; D004553:Electric Conductivity; D006801:Humans; D017136:Ion Transport; D018408:Patch-Clamp Techniques; D020545:Respiratory Mucosa / Q000166:cytology / Q000187:drug effects / Q000502:physiology*
D001426:Bacterial Proteins; C505032:CFTR protein, human; D002712:Chlorides; C074689:VacA protein, Helicobacter pylori; D019005:Cystic Fibrosis Transmembrane Conductance Regulator