title: Lack of enteral nutrition delays nuclear factor kappa B activation in peritoneal exudative cells in a murine glycogen-induced peritonitis model.
abstract: BACKGROUND
  Early enteral nutrition is associated with a lower incidence of intraabdominal abscess in severely injured patients than parenteral nutrition (PN). We explored the underlying mechanisms by examining the influence of nutrition route on nuclear factor kappaB (NFkappaB) activation in peritoneal exudative cells (PECs) and peritoneal cytokine levels.
  
  
  METHODS
  Thirty male Institute Cancer Research mice were randomized to chow (n = 10), IV PN (n = 10), or intragastric (IG) PN (n = 10) and fed for 5 days. PECs were harvested at 2 or 4 hours after intraperitoneal injection of 2 mL of 1% glycogen. Intranuclear NFkappaB activity in PECs was examined by laser scanning cytometry. Cytokine (tumor necrosis factor-alpha [TNF-alpha], macrophage inflammatory protein-2 [MIP-2], interleukin-10 [IL-10]) levels in peritoneal lavaged fluid were determined by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  Intranuclear NFkappaB at 2 hours was significantly higher in the chow and IG-PN groups than in the IV-PN group. TNF-alpha and IL-10 levels of the chow group were significantly higher than those of IV-PN mice at 2 hours, whereas those of IG-PN mice were midway between those of the chow and IV-PN groups. MIP-2 was significantly higher in the chow group than in the IG-PN and IV-PN mice at 2 hours. TNF-alpha levels correlated positively with intranuclear NFkappaB activity in PECs.
  
  
  CONCLUSIONS
  Enteral nutrition may improve peritoneal defense by preserving early NFkappaB activation in PECs and cytokine responses.
authors.affiliation: Department of Surgery I, National Defense Medical College, Tokorozawa, Saitama, Japan.
authors.forename: Chikara
authors.initials: C
authors.lastname: Ueno
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Fukatsu
authors.forename: Woodae
authors.initials: W
authors.lastname: Kang
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Maeshima
authors.forename: Hidetoshi
authors.initials: H
authors.lastname: Nagayoshi
authors.forename: Jiro
authors.initials: J
authors.lastname: Omata
authors.forename: Hideaki
authors.initials: H
authors.lastname: Saito
authors.forename: Hoshio
authors.initials: H
authors.lastname: Hiraide
authors.forename: Hidetaka
authors.initials: H
authors.lastname: Mochizuki
mesh_terms: D000818:Animals; D054426:Chemokine CXCL2; D016207:Cytokines / Q000378:metabolism*; D004195:Disease Models, Animal; D004333:Drug Administration Routes; D004750:Enteral Nutrition; D006003:Glycogen / Q000494:pharmacology*; D016753:Interleukin-10 / Q000378:metabolism; D047569:Laser Scanning Cytometry / Q000379:methods; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D015846:Monokines / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism*; D010288:Parenteral Nutrition / Q000009:adverse effects; D010529:Peritoneal Cavity / Q000166:cytology*; D010538:Peritonitis / Q000139:chemically induced / Q000276:immunology*; D011897:Random Allocation; D013047:Specific Pathogen-Free Organisms; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D054426:Chemokine CXCL2; D016207:Cytokines; D015846:Monokines; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D006003:Glycogen