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Enteral Feeding of a Chemically Defined Diet Preserves Pulmonary Immunity but Not Intestinal Immunity: The Role of Lymphotoxin β Receptor
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 antibacte...
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Published in: | JPEN. Journal of parenteral and enteral nutrition 2007-11, Vol.31 (6), p.477-481 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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 β receptor (LTβR) 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 LTβR 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 LTβR by Western blot.
Results: IV-PN significantly reduced intestinal and lung LTβR
compared with CED and chow. IG-PN reduced LTβR 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 LTβR expression, whereas intestinal
LTβR levels are maintained only with CEDs (chow and CED). We hypothesize
that LTβR 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.
Type and route of diet differentially influence molecular events in the gut and lung mucosal immune system. Any enteral feeding maintains lung lymphotoxin β receptor (LTβR) expression, an important control molecule for immune integrity, whereas intestinal expression requires a complex diet. LTβR explains preservation of respiratory tract immunity when intestinal immunity is compromised. |
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ISSN: | 0148-6071 1941-2444 |
DOI: | 10.1177/0148607107031006477 |