Targeting extracellular protein disulphide isomerase to control Burkholderia cenocepacia lung infections

Abstract

Background. We have shown that the interaction between Burkholderia cenocepacia and lung epithelial cells is mediated by redox sensitive enzymes of the protein disulphide isomerase (PDI) family, in particular by ERp57. In fact, either thiol reactive agents (DTT, GSH, and DTNB) or ERp57 inhibitors are able to drastically reduce the adhesion and the invasion of B. cenocepacia into epithelial cells and to attenuate the proinflammatory response elicited by bacteria. These observations suggest that defects in GSH export in the airway surface liquid, observed in cystic fibrosis (CF) patients, may favour B. cenocepacia infection.