Effect of route and type of nutrition on intestine-derived inflammatory responses

Immunological links between the gastrointestinal (GI) tract and respiratory tract has been postulated in the development and maintenance of mucosal immunity. Route and type of nutrition affects mucosal immunity by reducing cell populations within the Peyer's patches of the small intestine and lamina propria as well as altering cytokine profiles within these sites. In addition to the mucosal affects, these alternations in cytokines (decreases in interleukin-4 and interleukin-10) also appear to influence the vascular endothelium of the GI tract.

This review examines the laboratory data regarding cytokine profile within the gut, endothelial adhesion molecule expression within the intestinal and extraintestinal organs, and the effect of these alterations on neutrophil accumulation and organ responses to gut ischemia/reperfusion. It also describes the effect of a specific nutrient, glutamine, on the starved gut.

Changes induced by failure to feed the GI tract affects GI vascularity increasing expression of proinflammatory adhesion molecules. These adhesion molecules attract neutrophils and prime them for subsequent ischemic events. Lack of feeding the gastrointestinal tract acts as a "first hit" and increases the inflammatory response to a secondary insult in the lungs, liver, and GI tract. The addition of the specific nutrient, glutamine, reverses many of these defects and favorably influences the proinflammatory effects of gut starvation.