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Previous studies have demonstrated that extracellular glutathione reduces the ability of the Cystic Fibrosis pathogen  Burkholderia cenocepacia  to infect primary or immortalized epithelial respiratory cells. We report here that the adhesion and invasion ability of  B. cenocepacia  is limited also by thiol-oxidizing and disulphide-reducing agents and by protein disulfide isomerase (PDI) inhibitors. PDI inhibitors also reduce the proinflammatory response elicited by cells in response to  Burkholderia . These findings indicate that a membrane-associated PDI catalyzes thiol/disulphide exchange reactions which favor bacterial infection. The combined use of selective PDI inhibitors, RNA silencing and specific antibodies identified ERp57 as a major PDI involved in the interaction between  B. cenocepacia  and epithelial cells. This study contributes to the elucidation of the  Burkholderia  pathogenic mechanisms by showing that this microorganism exploits a membrane-associated host protein to infect epithelial cells and identifies ERp57 as a putative pharmacological target for the treatment of  Burkholderia  lung infections.

An ERp57-mediated disulphide exchange promotes the interaction between Burkholderia cenocepacia and epithelial respiratory cells