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 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.