title: Enteral nutrition rapidly reverses total parenteral nutrition-induced impairment of hepatic immunity in a murine model.
abstract: OBJECTIVE
  Total parenteral nutrition (TPN) impairs host immunocompetence, a mechanism possibly underlying the high morbidity of infectious complications in critically ill patients. Our recent study demonstrated TPN to reduce the number and function of hepatic mononuclear cells (MNCs) and to worsen survival after intraportal Pseudomonas challenge in mice. The present study examined the duration of enteral nutrition (EN) needed to reverse TPN-induced changes in hepatic MNCs in a murine model.
  
  
  METHODS
  Male ICR mice (6 weeks) received 5 days of TPN followed by 0 (TPN), 12 (EN12), 24 (EN24), 48 (EN48) or 72 (EN72)h of chow feeding. Control mice (Control) were given chow with intravenous saline infusions for 5 days. After nutritional support, hepatic MNCs were isolated and counted. Lipopolysaccharide (LPS) receptor expressions (CD14 and TLR4/MD2) on Kupffer cells were analyzed by flowcytometry. In addition, TPN, EN12, EN48 and control mice were given intraportal Pseudomonas challenge and survival was monitored.
  
  
  RESULTS
  The TPN group was significantly lower in hepatic MNC number and LPS receptor expressions than the Control group. However, EN quickly reversed TPN-induced hepatic impairments in MNC loss within 12h, CD14 expression within 48 h and TLR4/MD2 expression within 24h. Survival of the EN48 group was significantly improved as compared with the TPN and EN12 groups.
  
  
  CONCLUSIONS
  EN rapidly reverses TPN-induced impairment of hepatic immunity along with increased hepatic MNC numbers and LPS receptor expressions on Kupffer cells.
authors.affiliation: Department of Surgery, National Defense Medical College, Japan.
authors.forename: Jiro
authors.initials: J
authors.lastname: Omata
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Fukatsu
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Maeshima
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Moriya
authors.forename: Satoshi
authors.initials: S
authors.lastname: Murakoshi
authors.forename: Midori
authors.initials: M
authors.lastname: Noguchi
authors.forename: Koichi
authors.initials: K
authors.lastname: Okamoto
authors.forename: Satomi
authors.initials: S
authors.lastname: Fukazawa
authors.forename: Daizoh
authors.initials: D
authors.lastname: Saitoh
authors.forename: Hidetaka
authors.initials: H
authors.lastname: Mochizuki
authors.forename: Junji
authors.initials: J
authors.lastname: Yamamoto
authors.forename: Kazuo
authors.initials: K
authors.lastname: Hase
mesh_terms: D000818:Animals; D001835:Body Weight; D002452:Cell Count; D004195:Disease Models, Animal; D004750:Enteral Nutrition; D016867:Immunocompromised Host / Q000502:physiology*; D007728:Kupffer Cells / Q000378:metabolism / Q000502:physiology; D007963:Leukocytes, Mononuclear / Q000502:physiology; D018950:Lipopolysaccharide Receptors / Q000378:metabolism; D008099:Liver / Q000033:anatomy & histology / Q000166:cytology / Q000276:immunology*; D008214:Lymphocytes / Q000502:physiology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009929:Organ Size; D010289:Parenteral Nutrition, Total / Q000009:adverse effects*; D011552:Pseudomonas Infections / Q000276:immunology; D011550:Pseudomonas aeruginosa; D011897:Random Allocation; D016019:Survival Analysis; D013997:Time Factors; D051197:Toll-Like Receptor 4 / Q000378:metabolism
chemical_list: D018950:Lipopolysaccharide Receptors; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4