The Influence of Nutrition on Mucosal Immunology and Endothelial Cell Adhesion Molecules

The incidence of pneumonia and intra-abdominal abscess decreases when critically injured patients are fed enterally as opposed to intravenously or not at all [1, 2]. Our work has focused on mechanisms underlying these clinical findings. In attempting to determine how nutrient, hormonal, or pharmacologic manipulation improves immune dysfunction occurring in fasted or intravenously fed patients, the key question has been: Why does the route of nutrition impair respiratory tract defenses in critically ill patients? To pursue this issue one must understand the normal mechanisms of defense at mucosal surfaces. Our work has demonstrated a key link between the gastrointestinal tract and respiratory immunity with important observations that route of nutrition influences the structure and function of the gut-associated lymphoid tissue (GALT) [3]. GALT cellular changes influence the cytokine environment, IgA production, endothelial cell activation and recruitment.