title: Peritoneal fluid: a potential mechanism of systemic neutrophil priming in experimental intra-abdominal sepsis.
abstract: BACKGROUND
  Recent studies suggest that peritoneal fluid (PF) may be an important mediator of inflammation. The aim of this study was to test the hypothesis that PF may drive systemic inflammation in intra-abdominal sepsis by representing a priming agent for neutrophils.
  
  
  METHODS
  PF was collected 12 hours after the initiation of intra-abdominal sepsis in swine. Naive human neutrophils were primed with PF before treatment with N-formyl-Met-Leu-Phe or phorbol 12-myristate 13-acetate to elucidate receptor-dependent and receptor-independent mechanisms of neutrophil activation. Flow cytometry was used to quantify neutrophil surface adhesion marker expression of integrins and selectins and superoxide anion production. Additionally, proinflammatory cytokines were quantified in PF.
  
  
  RESULTS
  PF primed neutrophils via receptor-dependent and receptor-independent mechanisms. There were significant increases in the proinflammatory cytokines interleukin-6 and tumor necrosis factor-α in PF correlating with the development of intra-abdominal sepsis.
  
  
  CONCLUSIONS
  PF represents a priming agent for naive polymorphonuclear cells in intra-abdominal sepsis. This may be secondary to increased levels of proinflammatory cytokines. Strategies to reduce the amount of PF may decrease the systemic inflammatory response by reducing a priming agent for neutrophils.
authors.affiliation: Departments of Pediatric Surgery and Surgery, University of Texas Medical School at Houston, USA.
authors.forename: Shinil K
authors.initials: SK
authors.lastname: Shah
authors.forename: Fernando
authors.initials: F
authors.lastname: Jimenez
authors.forename: Peter A
authors.initials: PA
authors.lastname: Walker
authors.forename: Hasen
authors.initials: H
authors.lastname: Xue
authors.forename: Teri D
authors.initials: TD
authors.lastname: Feeley
authors.forename: Karen S
authors.initials: KS
authors.lastname: Uray
authors.forename: Kenneth C
authors.initials: KC
authors.lastname: Norbury
authors.forename: Randolph H
authors.initials: RH
authors.lastname: Stewart
authors.forename: Glen A
authors.initials: GA
authors.lastname: Laine
authors.forename: Charles S
authors.initials: CS
authors.lastname: Cox
mesh_terms: D000818:Animals; D001202:Ascitic Fluid / Q000276:immunology*; D039481:CD11b Antigen / Q000378:metabolism; D018821:CD18 Antigens / Q000378:metabolism; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism; D059413:Intraabdominal Infections / Q000276:immunology*; D019041:L-Selectin / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism*; D018805:Sepsis / Q000276:immunology*; D013481:Superoxides / Q000378:metabolism; D013552:Swine; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D039481:CD11b Antigen; D018821:CD18 Antigens; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D013481:Superoxides; D019041:L-Selectin