Lack of Enteral Nutrition Delays Nuclear Factor Kappa B Activation in Peritoneal Exudative Cells in a Murine Glycogen-Induced Peritonitis Model

• Published in: JPEN. Journal of parenteral and enteral nutrition 2006-05, Vol.30 (3), p.179-185
• Main Authors: Ueno, Chikara, Fukatsu, Kazuhiko, Kang, Woodae, Maeshima, Yoshinori, Nagayoshi, Hidetoshi, Omata, Jiro, Saito, Hideaki, Hiraide, Hoshio, Mochizuki, Hidetaka
• Format: Article
• Language: English
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Biological and medical sciences; Blood and lymphatic vessels; Blood. Blood and plasma substitutes. Blood products. Blood cells. Blood typing. Plasmapheresis. Apheresis; Cardiology. Vascular system; Chemokine CXCL2; Cytokines - metabolism; Disease Models, Animal; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous; Drug Administration Routes; Emergency and intensive care: metabolism and nutrition disorders. Enteral and parenteral nutrition; Enteral Nutrition; Glycogen - pharmacology; Intensive care medicine; Interleukin-10 - metabolism; Laser Scanning Cytometry - methods; Male; Medical sciences; Mice; Mice, Inbred ICR; Monokines - metabolism; NF-kappa B - metabolism; Parenteral Nutrition - adverse effects; Peritoneal Cavity - cytology; Peritonitis - chemically induced; Peritonitis - immunology; Random Allocation; Specific Pathogen-Free Organisms; Transfusions. Complications. Transfusion reactions. Cell and gene therapy; Tumor Necrosis Factor-alpha - metabolism
• ISSN: 0148-6071; 1941-2444
• DOI: 10.1177/0148607106030003179

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 κB (NFκB) 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 NFκB activity in PECs was examined by laser scanning cytometry. Cytokine (tumor necrosis factor-α [TNF-α], macrophage inflammatory protein-2 [MIP-2], interleukin-10 [IL-10]) levels in peritoneal lavaged fluid were determined by enzyme-linked immunosorbent assay. Results: Intranuclear NFκB at 2 hours was significantly higher in the chow and IG-PN groups than in the IV-PN group. TNF-α 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-α levels correlated positively with intranuclear NFκB activity in PECs. Conclusions: Enteral nutrition may improve peritoneal defense by preserving early NFκB activation in PECs and cytokine responses. We clarified an important mechanism for impaired peritoneal defense during lack of enteral nutrition. Parenterally fed mice showed delay of NFκB activation in peritoneal exudative cells and cytokine responses in glycogen-induced peritonitis, as compared with enterally fed animals.