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 pro-inflammatory 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.

Hypothesis and objectives. ERp57 inhibitors, in particular epigallocatechin-3-gallate (EGCG), the most abundant green tea catechin, could be useful in therapies aimed at controlling Burkholderia lung infection in CF patients. To this aim we have evaluated: 1) the effect of EGCG on Burkholderia infection in different cell types; 2) the effect of EGCG on Burkholderia intracellular replication; 3) the efficacy of EGCG in infected mice.