title: Extracellular glutathione decreases the ability of Burkholderia cenocepacia to penetrate into epithelial cells and to induce an inflammatory response.
abstract: BACKGROUND
  The airway surface liquid (ASL) of Cystic Fibrosis (CF) patients contains a lower concentration of reduced glutathione (GSH) with respect to healthy people. It is not known whether this defect may favor lung colonization by opportunistic pathogens.
  
  
  RESULTS
  We have analyzed the effects of extracellular GSH on the ability of Burkholderia cenocepacia to penetrate and multiply in epithelial respiratory cells. Extracellular GSH proved to be able to drastically reduce the pathogen ability to adhere and invade airway epithelial cells. This effect is correlated to a GSH-dependent increase in the number of free thiols on the surface of epithelial cells, suggestive of a change in the oxidoreductive status of membrane proteins involved in B. cenocepacia recognition. Moreover, treatments with GSH led to a consistent reduction of the expression of IL-8, TNF-α and IL-1β in response to B. cenocepacia infection.
  
  
  CONCLUSIONS
  Extracellular GSH modulates the interaction between B. cenocepacia and epithelial respiratory cells and inhibits the bacterial invasion into these cells. This suggests that therapies aimed at restoring normal levels of GSH in the ASL might be beneficial to control CF lung infections.
authors.affiliation: Istituto di Ricovero e Cura a Carattere Scientifico San Raffaele Pisana, Roma, Italy.
authors.forename: Melania
authors.initials: M
authors.lastname: D'Orazio
authors.forename: Francesca
authors.initials: F
authors.lastname: Pacello
authors.forename: Andrea
authors.initials: A
authors.lastname: Battistoni
mesh_terms: D001980:Bronchi / Q000187:drug effects / Q000382:microbiology; D019121:Burkholderia Infections / Q000150:complications / Q000188:drug therapy / Q000382:microbiology; D057508:Burkholderia cenocepacia / Q000187:drug effects* / Q000502:physiology; D002460:Cell Line; D003550:Cystic Fibrosis / Q000150:complications / Q000188:drug therapy / Q000382:microbiology; D004847:Epithelial Cells / Q000187:drug effects* / Q000382:microbiology / Q000473:pathology; D005978:Glutathione / Q000494:pharmacology*; D054884:Host-Pathogen Interactions / Q000187:drug effects*; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000188:drug therapy / Q000382:microbiology; D053583:Interleukin-1beta / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D016209:Interleukin-8 / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D010084:Oxidation-Reduction / Q000187:drug effects; D061251:Primary Cell Culture; D020545:Respiratory Mucosa / Q000187:drug effects* / Q000382:microbiology / Q000473:pathology; D014132:Trachea / Q000187:drug effects / Q000382:microbiology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000096:biosynthesis
chemical_list: D053583:Interleukin-1beta; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D005978:Glutathione