Lack of enteral nutrition delays nuclear factor kappa B activation in peritoneal exudative cells in a murine glycogen-induced peritonitis model.

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.