Nutrition and gut immunity

Abstract

The human intestine contains huge amounts of nonpathologic bacteria surviving in an environment that is beneficial to both the host and the bacterial populations. When short pauses in oral intake occur with minimal alterations in the mucosa-microbial interface, critical illness, with its attendant acidosis, prolonged gastrointestinal tract starvation, exogenous antibiotics, and breakdown in mucosal defenses, renders the host vulnerable to bacterial challenge and also threatens the survival of the bacteria. This review examines the altered innate and adaptive immunologic host defenses that occur as a result of altered oral or enteral intake and/or injury.

Figure 1. Gut associated lymphoid tissue (GALT) and systemic mucosal immunity

GALT is a center of systemic mucosal immunity. Naïve lymphocytes are sensitized at Peyer’s patches, migrate to mesenteric lymph nodes, enter to systemic circulation via thoracic duct, and home to mucosal sites.

Figure 2. Mechanisms underlying impaired immunity during gut starvation

Impairment of gut immunity due to gut starvation is related to reduced LTβR expression, ERK phosphorylation, IL-7 production and other factors.

Figure 3. Influence of gut starvation on peritoneal host defense

Gut starvation blunts NFκB activation in peritoneal resident macrophages and exudative neutrophils, impairing peritoneal host defense against bacterial contamination.

Figure 4. Influences of gut starvation on host immunity and inflammation

Gut starvation impairs various host defense systems, while causing inappropriate activation of endothelial cells.