Impact of the feeding route on gut mucosal immunity

Enteral nutrition is recommended as a standard nutritional therapy in clinical settings. The rationale behind enteral nutrition may be decreased infectious morbidities compared with parenteral nutrition. However, the mechanism may not be well understood.

Animal studies have revealed that enteral nutrition, compared with parenteral nutrition, preserves the gut-associated lymphoid tissue mass and function with well controlled gut cytokine milieu and intracellular signaling pathway, leading to the maintenance of intestinal and extraintestinal acquired mucosal immunity. Moreover, enteral nutrition can enhance the gut innate immunity by increasing the antimicrobial peptides, such as secretory phospholipase A2. More importantly, a recent clinical study demonstrated preoperative parenteral nutrition without enteral nutrition to decrease the number of T cells, IgA-producing cells, and mature dendritic cells in human terminal ileum, which are consistent with the data obtained from animal studies. Investigation of the mechanism has given us some surrogates of enteral nutrition during parenteral nutrition, such as glutamine, butyric acid, cytokines, and other mediators. However, to date, no surrogates can restore parenteral-nutrition-induced impairment of host defense completely.

Because enteral nutrition is a practical way to preserve gut immunity, clinicians should make any efforts to shorten the period of enteral nutrition absence and increase the dose according to the degree of tolerance.