Commensal Bacteria of the GI Tract: Benefits of Probiotic Supplementation (post 3)

INTESTINAL MICROBES AND IMMUNITY

The GI tract contains approximately 70% of our immune system.²⁹ For example, the gut-associated lymphoid tissues (GALT), which include the appendix and Peyer’s patches, contain more lymphocytes than all of the secondary lymphoid organs combined (spleen, lymph nodes, other mucosa-associated lymphoid tissues).³⁰ This makes sense because the mouth is the major portal through which foreign objects (food, water, microbes, toxins, etc.) enter the body, and the way the GI system deals with is a major determinant of our health status. Nutrients and other benign substances must be recognized as molecules that do not necessitate an immune response. Bacteria, viruses, fungi, protozoa, etc., must be identified as either “friendly” or “unfriendly” and dealt with accordingly. Because of the overwhelming population of microbes in the GI tract, the immune system must learn early on what is normal and what is not. This necessitates early establishment of normal, healthful microbial populations.

Normal GI microflora populations are crucial for the maturation of acquired immunity. Beneficial intestinal bacteria can stimulate the synthesis and secretion of IgA, the antibody that coats and protects mucosal surfaces against microbial infection.³¹ The GI microflora also assists development of normal immunity by its effects on antigen-presenting cells. Antigen-presenting cells are immune cells (macrophages, B lymphocytes, dendritic cells, etc.) that process antigens (foreign molecules that cause an immune response), then present them to T helper (T_H) cells for recognition and appropriate response. Antigen-presenting cells also secrete chemicals that help stimulate T_H cell response. Dendritic cells are the antigen-presenting cells of the colon. They are generally believed to derive from monocytes, a type of white blood cell, that differentiate into antigen-presenting cells that reside in the lamina propria (the layer of the colon wall just beneath the mucosal surface) and extend their dendrites (long, fingerlike projections) through the epithelial cell layer into the lumen of the gut. When a dendrite comes in contact with an antigen, it ingests it by phagocytosis or endocytosis, then presents the antigen to a T_H cell that also resides within the lamina propria. The T_H cell then determines whether or not the antigen requires further attention, and appropriate action can be initiated.

A study demonstrated the specificity of colonic dendrites regarding their reaction to various species of bacteria found in the gut. Undifferentiated human monocytes produced higher levels of interleukin-12p70 (IL-12p70) and tumor necrosis factor (TNF) in response to Lactobacillus plantarum and Bifidobacterium adolescentis, two healthful colonic bacteria, than to potentially pathogenic Escherichia coli and Veillonella parvula. On the other hand, human monocytes that had differentiated into dendritic cells in the gut secreted large amounts of IL-12p70, TNF, IL-6 and IL-10 in response to E. coli and V. parvula, but were practically non-responsive to L. plantarum and B. adolescentis. This evidence suggests that dendritic cells in the gut recognize and respond to potential pathogenic bacteria, but do not respond to healthful bacteria.¹¹

A balanced T_H cell response is also important. The T_H1 subset of lymphocytes is responsible for many cell-mediated responses, and is associated with promotion of excessive inflammation and tissue injury. The T_H2 subset promotes the humoral (antibody) response, and supports allergic reactions. Therefore, an imbalance favoring a T_H1 response can contribute to inflammatory bowel diseases, and an imbalance that favors the T_H2 response can promote atopic diseases.³² Appropriate colonization of GI microbes with probiotics helps to maintain proper T_H cell responses, thus reducing the risk of these diseases.³¹

The means by which the microflora assists proper immune development is not fully understood, although it now known that polysaccharides play a critical part in this process. For example, colonization of just one species, a human commensal bacterium, Bacteroides fragilis, in germ-free mice was sufficient to correct T cell deficiencies normally seen in these animals. But more than that, investigators discovered that a polysaccharide found on its cell wall was the critical factor in orchestrating lymphoid organogenesis and correcting T cell deficiencies and T_H1/T_H2 imbalances (Figure B).³³ Isolating the particular polysaccharide and introducing it to the animals without concurrent colonization with B. fragilis produced the same results. Thus, at least in this case, a bacterial carbohydrate is the requisite molecular entity for the proper development of the immune system.

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