Loss of upper respiratory tract immunity with parenteral feeding

The authors examine the effect of route and type of nutrition on an established upper respiratory tract immunity and investigate potential mechanisms for increased pneumonia rates in critically injured patients fed parenterally.

The primary immunologic defense against many mucosal infections is IgA. Prior work shows that mice fed total parenteral nutrition (TPN) solutions either intravenously or intragastrically had small intestinal gut-associated lymphoid tissue (GALT) atrophy along with decreased intestinal IgA compared with animals fed complex enteral diets. The small intestine is postulated to be the origin of most mucosal immunity, both intraintestinal and extraintestinal. The impact of diets affecting GALT, small intestine IgA, and upper respiratory tract immunity is studied.

Male Institute of Cancer Research mice underwent intranasal inoculation with a mouse-specific influenza virus to establish immunity. Three weeks later, the mice were randomized to chow, intragastric Nutren (Clintec, Chicago, IL), intravenous TPN, or intragastric TPN. After 5 days of feeding, mice were challenged with intranasal virus and killed at 40 hours to determine viral shedding from the upper respiratory tract.

Despite similar body weights, there was significant atrophy in the Peyer's patch cells from animals fed the TPN solution intravenously or intragastrically. There was no viral shedding in any animal fed via the gastrointestinal tract, whereas 5 of 10 animals fed intravenous TPN had continued viral shedding.

The IgA-dependent upper respiratory tract immunity was preserved with enteral feeding but not with intravenous feeding. Upper respiratory tract immunity is not dependent on intestinal GALT mass but is influenced by route of nutrition. The underlying mechanisms may explain the higher pneumonia rate in critically injured patients fed parenterally.