title: Enteral feeding of a chemically defined diet preserves pulmonary immunity but not intestinal immunity: the role of lymphotoxin beta receptor.
abstract: BACKGROUND
  Compared with chow or a complex enteral diet (CED), IV administration of a parenteral nutrition solution (IV-PN) impairs intestinal and respiratory mucosal immunity, resulting in cellular and immunoglobulin A (IgA) defects in the intestine and impaired respiratory antiviral and antibacterial defenses. PN given intragastrically (IG-PN) impairs intestinal immunity similar to IV-PN but preserves antiviral defences and partially preserves antibacterial defenses. Lymphotoxin beta receptor (LTbetaR) is a molecule essential for development and organization of lymphoid tissue. It controls many molecules important in mucosal immune integrity. This study examines effects of route (IV or enteral) and type (PN, CED, or chow) on murine intestine and lung LTbetaR expression.
  
  
  METHODS
  Forty-three mice randomly received IV-PN (n = 12), IG-PN (n = 11), IV saline + chow (chow; n = 11), or a CED (n = 9). After 5 days of feeding, intestinal and lung samples were obtained and processed for levels of LTbetaR by Western blot.
  
  
  RESULTS
  IV-PN significantly reduced intestinal and lung LTbetaR compared with CED and chow. IG-PN reduced LTbetaR levels only in the intestine but preserved lung levels.
  
  
  CONCLUSIONS
  Route and type of nutrition differentially influence molecular events in the intestinal and respiratory mucosal immune systems. Enteral feeding with any diet (complex or chemically defined) maintains lung LTbetaR expression, whereas intestinal LTbetaR levels are maintained only with CEDs (chow and CED). We hypothesize that LTbetaR is responsible for the observed preservation of respiratory tract immunity with administration of a noncomplex, chemically defined enteral diet, whereas intestinal immunity is compromised with this diet.
authors.affiliation: Veterans Administration Surgical Services, William S. Middleton Memorial Veterans Hospital, Madison, Wisconsin, USA. kudsk@surgery.wisc.edu
authors.forename: Kenneth A
authors.initials: KA
authors.lastname: Kudsk
authors.forename: F Enrique
authors.initials: FE
authors.lastname: Gomez
authors.forename: Woodae
authors.initials: W
authors.lastname: Kang
authors.forename: Chikara
authors.initials: C
authors.lastname: Ueno
mesh_terms: D000818:Animals; D015153:Blotting, Western; D004333:Drug Administration Routes; D004750:Enteral Nutrition; D005786:Gene Expression Regulation; D018928:Immunity, Mucosal / Q000187:drug effects* / Q000502:physiology; D007070:Immunoglobulin A / Q000096:biosynthesis; D007136:Immunoglobulins / Q000096:biosynthesis; D007262:Infusions, Intravenous; D007413:Intestinal Mucosa / Q000378:metabolism*; D007421:Intestine, Small / Q000276:immunology; D008168:Lung / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D053259:Lymphotoxin beta Receptor / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D010288:Parenteral Nutrition; D010581:Peyer's Patches / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D011897:Random Allocation
chemical_list: D007070:Immunoglobulin A; D007136:Immunoglobulins; D053259:Lymphotoxin beta Receptor