Document Detail


Route and type of nutrition influence nuclear factor kappaB activation in peritoneal resident cells.
MedLine Citation:
PMID:  16205325     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Chikara Ueno; Kazuhiko Fukatsu; Woodae Kang; Yoshinori Maeshima; Tomoyuki Moriya; Etsuko Hara; Hidetoshi Nagayoshi; Jiro Omata; Hideaki Saito; Hoshio Hiraide; Hidetaka Mochizuki
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Shock (Augusta, Ga.)     Volume:  24     ISSN:  1073-2322     ISO Abbreviation:  Shock     Publication Date:  2005 Oct 
Date Detail:
Created Date:  2005-10-05     Completed Date:  2006-02-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9421564     Medline TA:  Shock     Country:  United States    
Other Details:
Languages:  eng     Pagination:  382-7     Citation Subset:  IM    
Affiliation:
Department of Surgery I, National Defense Medical College, Saitama, Japan.
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MeSH Terms
Descriptor/Qualifier:
Active Transport, Cell Nucleus
Amino Acids / chemistry
Animals
Body Weight
Cytoplasm / metabolism
Dose-Response Relationship, Drug
Enzyme-Linked Immunosorbent Assay
Inflammation
Lasers
Lipopolysaccharides / chemistry,  metabolism
Macrophages / metabolism
Mice
Microscopy, Fluorescence
NF-kappa B / metabolism*
Peritoneum / immunology,  pathology*
Protein Transport
Sepsis
Time Factors
Tumor Necrosis Factor-alpha / metabolism
Wound Healing
Chemical
Reg. No./Substance:
0/Amino Acids; 0/Lipopolysaccharides; 0/NF-kappa B; 0/Tumor Necrosis Factor-alpha

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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