title: Lack of enteral feeding increases expression of E-selectin after LPS challenge.
abstract: BACKGROUND
  Total parenteral nutrition (IV-TPN) increases neutrophil accumulation in the small intestine, expression of intestinal ICAM-1 and P-selectin, and upregulates E-selectin expression in the lung. Endothelial activation induced by lack of enteral nutrition may change the response to injury or infection. This study investigated whether nutrition influenced the expression of the adhesion molecule, E-selectin and ICAM-1, following endotoxin challenge.
  
  
  METHODS
  Forty-three mice were injected with saline, 2, 20, 200, 2000, or 10000 microg/kg lipopolysaccharide (LPS) intraperitoneally. E-selectin expression in the lung, small intestine, and heart was quantified at 3 h after challenge, while ICAM-1 was measured at 5 h, using the dual-radiolabeled monoclonal antibody technique. Next, 80 mice were fed chow, intragastric (IG)-TPN, or IV-TPN for 5 days, and then received intraperitoneal 2 or 200 microg/kg LPS. E-selectin and ICAM-1 expression in organs was measured at 3 and 5 h after endotoxin, respectively.
  
  
  RESULTS
  E-selectin expression in organs increased LPS dose dependently. ICAM-1 levels reached early peaks in the lung and in the intestine. Also, IV-TPN significantly increased E-selectin expression in the small intestine and tended to increase pulmonary E-selectin, when compared to chow or IG-TPN animals. There were no significant differences in E-selectin expression among three diet groups after 200 microg/kg LPS challenge. No differences in ICAM-1 expression were observed in any organ among the three groups after 2 or 200 microg/kg LPS injection.
  
  
  CONCLUSIONS
  E-selectin rather than ICAM-1, because of the expression pattern after various dosages of LPS challenge, may be a determining factor for the degree of LPS-induced inflammation at the early phase. Lack of enteral nutrition may increase inflammatory response through enhanced gut E-selectin levels after a small dose of LPS.
authors.affiliation: Department of Surgery, The University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA.
authors.forename: K
authors.initials: K
authors.lastname: Fukatsu
authors.forename: B L
authors.initials: BL
authors.lastname: Zarzaur
authors.forename: C D
authors.initials: CD
authors.lastname: Johnson
authors.forename: A H
authors.initials: AH
authors.lastname: Lundberg
authors.forename: M K
authors.initials: MK
authors.lastname: Hanna
authors.forename: H G
authors.initials: HG
authors.lastname: Wilcox
authors.forename: K A
authors.initials: KA
authors.lastname: Kudsk
mesh_terms: D000818:Animals; D001835:Body Weight; D004305:Dose-Response Relationship, Drug; D019040:E-Selectin / Q000096:biosynthesis*; D004750:Enteral Nutrition; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D007421:Intestine, Small / Q000378:metabolism; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000494:pharmacology*; D008168:Lung / Q000378:metabolism; D051379:Mice; D008813:Mice, Inbred ICR; D010288:Parenteral Nutrition
chemical_list: D019040:E-Selectin; D008070:Lipopolysaccharides; D018799:Intercellular Adhesion Molecule-1