Is there evidence that the gut contributes to mucosal immunity in humans?

Our understanding of the common mucosal immune system derives from animal studies. Antigen-sensitized lymphocytes in the gut-associated lymphoid tissue (GALT) migrate via the blood to mucosal tissues to generate the mucosal-associated lymphoid tissue (MALT). In these sites, B cells differentiate into plasma cells and produce antigen-specific secretory IgA, the principal specific immune antiviral and antibacterial defense of moist mucosal surfaces. Responses to oral intake seem necessary to actively maintain this system in health. Experimentally, lack of enteral stimulation with parenteral feeding alters GALT and MALT size and function. These alterations disturb intestinal and extraintestinal mucosal immunity.

This review is an overview of current and classical studies demonstrating the human mucosal immune system and interactions with nutrition.

Human evidence of the mucosal immune system exists, although most data are indirect. Gut stimulation after oral intake induces a generalized immune response in the human MALT through a mucosal-immune network. Examples include neonatal development of GALT influenced by enteral feeding, the presence of antigen-specific IgA and antigen-specific IgA-secreting plasma cells in distant mucosal effector sites such as the breast after gut luminal antigen exposure, and isolation of IgA-producing cells from circulating blood.

It is unlikely that clinical studies will ever completely define the effect of route of feeding in all patient populations. This may be possible, however, if investigators understand, define and characterize nutrition-dependent immunologic mechanisms, allowing clinicians to examine clinical responses to nutrition in specific patient populations. This might allow generation of new approaches to protect mucosal immunity.