title: Route and type of nutrition influence nuclear factor kappaB activation in peritoneal resident cells.
abstract: Morbidity of intra-abdominal abscess is increased when severely injured patients are fed parenterally. Lack of enteral nutrition appears to impair peritoneal cavity host defense. Because the transcription factor nuclear factor kappaB (NFkappaB) regulates various genes involved in inflammatory responses and its activation is important for host defense, we hypothesized that enteral nutrition would preserve appropriate NFkappaB activation in peritoneal resident cells (PRCs), the first defense line against peritoneal contamination. Mice (n = 105) were randomized to chow (n = 38), intravenous (IV)-total parenteral nutrition (TPN) (n = 34), or intragastric (IG)-TPN (n = 33) for 5 days' feeding. In experiment 1, PRCs were harvested for measurement of intranuclear NFkappaB activity with or without in vitro lipopolysaccharide (LPS) stimulation using laser scanning cytometry and enzyme-linked immunoabsorbant assay. PRC numbers tended to be higher in enterally fed mice than in IV-TPN mice. The main PRC subpopulation was macrophages in all groups. NFkappaB activation was increased in response to LPS in chow mice, whereas there was no increase in the IV-TPN group. IG-TPN mice demonstrated moderate NFkappaB activation. In experiment 2, mice underwent cecal ligation and puncture (CLP). Survival was observed up to 5 days. In another set of mice, tumor necrosis factor (TNF) alpha levels of peritoneal lavaged fluid were measured 4 h after CLP. Survival times after CLP improved in the chow and IG-TPN groups compared with the IV-TPN group. TNFalpha levels were significantly higher in the chow than in the IV-TPN group. In conclusion, parenteral nutrition decreases PRC number and blunts NFkappaB activation in PRCs. These changes may impair host defense in the peritoneal cavity.
authors.affiliation: Department of Surgery I, National Defense Medical College, 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: Tomoyuki
authors.initials: T
authors.lastname: Moriya
authors.forename: Etsuko
authors.initials: E
authors.lastname: Hara
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: D021581:Active Transport, Cell Nucleus; D000596:Amino Acids / Q000737:chemistry; D000818:Animals; D001835:Body Weight; D003593:Cytoplasm / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004797:Enzyme-Linked Immunosorbent Assay; D007249:Inflammation; D007834:Lasers; D008070:Lipopolysaccharides / Q000737:chemistry / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism; D051379:Mice; D008856:Microscopy, Fluorescence; D016328:NF-kappa B / Q000378:metabolism*; D010537:Peritoneum / Q000276:immunology / Q000473:pathology*; D021381:Protein Transport; D018805:Sepsis; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014945:Wound Healing
chemical_list: D000596:Amino Acids; D008070:Lipopolysaccharides; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha