title: Surgical injury and metabolic stress enhance the virulence of the human opportunistic pathogen Pseudomonas aeruginosa.
abstract: BACKGROUND
  We have shown previously that the PA-I lectin of Pseudomonas aeruginosa plays a key role in gut-derived sepsis during surgical stress. The aims of this study were to determine if the intestinal tract lumen of a stressed host contained soluble factors that could induce the expression of PA-I.
  
  
  METHODS
  Mice were subjected to either 30% surgical hepatectomy or sham-laparotomy, and P. aeruginosa was introduced into the cecum. Twenty-four hours later, feces were recovered, and PA-I and exotoxin A were determined by real-time polymerase chain reaction (PCR). In reiterative experiments, fecal filtrates from both hepatectomy and sham-operated mice were tested for their ability to induce PA-I expression in cultures of P. aeruginosa. Finally, the media from cultured human intestinal epithelial (Caco-2) cells stressed with excess glutamine was tested for its ability to induce the expression of PA-I in cultures of P. aeruginosa.
  
  
  RESULTS
  Both PA-I and exotoxin A mRNA were increased in vivo in the intestinal tract of mice subjected to 30% hepatectomy. Soluble fecal filtrates from hepatectomy mice induced PA-I in vitro. Media from epithelial cells exposed to excess glutamine alone induced PA-I expression.
  
  
  CONCLUSIONS
  The intestinal environment of a stressed host contains soluble factors capable of inducing lethal virulence traits in human opportunistic pathogen P. aeruginosa.
authors.affiliation: Department of Surgery, University of Chicago, Chicago, Illinois 60637, USA.
authors.forename: Licheng R
authors.initials: LR
authors.lastname: Wu
authors.forename: Olga
authors.initials: O
authors.lastname: Zaborina
authors.forename: Alex
authors.initials: A
authors.lastname: Zaborin
authors.forename: Eugene B
authors.initials: EB
authors.lastname: Chang
authors.forename: Mark
authors.initials: M
authors.lastname: Musch
authors.forename: Christopher
authors.initials: C
authors.lastname: Holbrook
authors.forename: Jerrold R
authors.initials: JR
authors.lastname: Turner
authors.forename: John C
authors.initials: JC
authors.lastname: Alverdy
mesh_terms: D018829:Adhesins, Bacterial / Q000096:biosynthesis*; D000818:Animals; D002460:Cell Line; D004731:Endotoxins / Q000096:biosynthesis*; D005243:Feces / Q000737:chemistry / Q000382:microbiology; D006801:Humans; D037102:Lectins / Q000096:biosynthesis*; D051379:Mice; D023421:Models, Animal; D011552:Pseudomonas Infections / Q000209:etiology / Q000503:physiopathology*; D011550:Pseudomonas aeruginosa / Q000378:metabolism*; D013312:Stress, Physiological / Q000150:complications / Q000378:metabolism*; D013514:Surgical Procedures, Operative / Q000009:adverse effects; D014774:Virulence / Q000502:physiology
chemical_list: D018829:Adhesins, Bacterial; D004731:Endotoxins; D037102:Lectins; C038692:adhesin, Pseudomonas