Digestive Wellness: Strengthen the Immune System and Prevent Disease Through Healthy Digestion, Fourth Edition (44 page)

Regulatory system:
You also have a stop button that suppresses your immune system, called the regulatory system, which signals your body that all is well again. T cells are produced in the thymus and are called regulatory T cells (T-reg), also known as suppressor T cells, CD4, CD25, IL-10, and TGF-beta.

Of course, this all sounds nice and neat, but there is a lot of interplay and it’s not all cut and dried.

Throughout our digestive systems we have immune tissue called gut-associated lymphoid tissue (GALT). In the mucosal lining of the digestive lumen we have mucosal-associated lymphoid tissue (MALT). The MALT also encompasses your
nose, your bronchia, and in women the vulvo-vaginal areas. Altogether, 70 percent of your immune system lies within the GALT and digestive MALT and it protects us from antigens and other foreign invaders. Your tonsils, appendix, and the Peyer’s patches within the small intestine are examples of your GALT.

The GALT comprises two-thirds of the immune system in our bodies. It’s function is to absorb nutrients. The health of the GALT and MALT correlates with our own health. If these membranes are structurally strong, then our ability to withstand the stressors of life holds true. If these surfaces are compromised, then bacteria, antigenic food particles, and other inappropriate molecules get into our blood.

Secretory IgA (sIgA) is the major way that the MALT conveys the message of immune assault. Secretory IgA is a group of antibodies in the gut mucosa that, like sentinels, are on constant alert for foreign substances. When challenged by foreign molecules, sIgA forms immune complexes with allergens and microbes. I think of immune complexes as clumps of IgA or IgG antibodies that signal the immune system to respond. If these immune complexes get deposited in organs, they can cause disease themselves. Some IgA diseases include IgA nephropathy, vasculitis, lupus, rheumatoid arthritis, scleroderma, and Sjögren’s syndrome. Immune complexes signal cytokines to begin the inflammatory process designed to rid our bodies of antigenic materials, a response of the adaptive immune system. Without sufficient sIgA, the MALT cannot work properly.

Antibody reactions occur in stages. The initial response is sIgA. This is a nonspecific response. I like to think of IgA as a scout that stays outside looking for trouble. Continuing the first line of defense are the IgM antibodies. IgM antibodies are memory cells that are available for a short while. Like a temp worker, they have a memory of a specific assault and stay active until the IgG system kicks in. The secondary line of defense initiates the IgG response. IgG antibodies stay in the body for a long time or even a lifetime and are specific to foods and other molecules. They are like the guards on the castle wall and inside the gates. They respond to “enemy” molecules, while letting “friendly” molecules come inside the castle easily. Should the IgG antibodies become overwhelmed, IgE antibodies, true allergies, kick in. Evidence suggests that people don’t develop true IgE allergies until all of the other systems have broken down. When food sensitivities are cleared up, often IgE allergies also partially or fully resolve.

Deficiency of sIgA is the most common immunodeficiency. Low levels of sIgA make us more susceptible to infection and may be a fundamental cause of asthma, autoimmune diseases, candidiasis, celiac disease, chronic infections, food allergies, and more. In other words, if the sentry isn’t standing at the gate, anyone can come in! A study examining people with Crohn’s disease or ulcerative colitis found that
all of them had low levels of sIgA. It concluded that raising sIgA levels might eliminate inflammatory bowel disease. Chronic stress, adrenal insufficiencies, oral bacteria, recurring infection, leaky gut, celiac disease, Crohn’s disease, viruses such as newborn rubella and Epstein-Barr, immune hypersensitivity, and anti-inflammatory drugs can lower sIgA.

High levels of sIgA are found in people who have chronic infections and whose immune systems are overloaded. It often accompanies chronic viral infections like cytomegalovirus (CMV), Epstein-Barr virus, and HIV. It has also been found in people with rare medical problems like Berger’s nephropathy, dermatitis herpetiformis, gingivitis, hepatic glomerulonephritis, IgA neoplasms, parotitis, and anti-sperm antibodies. Factors that increase sIgA include acute stress, chronic infections, heavy smoking, alcoholism, periodontal disease, dental plaque accumulation, leaky gut, and throat cancer.

When microbes enter the digestive system, they are confronted with several nonspecific and antigen-specific defense mechanisms (innate immune system) including peristalsis, bile secretion, hydrochloric acid, mucus, antibacterial peptides, and IgA. This stops most microbes and parasites from infecting the body.

The mucosal surface of the gut lining is only one cell thick. Underneath this is the GALT. If the digestive system is presented with a foreign substance, an antigen, specialized cells called M-cells carry the antigen to the lining of the digestive tract. There they are “checked out,” or sampled, by specialized cells called Peyer’s patches in the intestinal lining. These cells in turn alert B and T cells to begin processing the antigens. The B and T cells carry the antigens back to the intestinal mucosa, where they are gobbled up by macrophages, part of the innate immune system.

We also have pattern recognition substances, lectins and toll-like receptors, that help us recognize friend from foe. The toll-like receptors (TLRs) act as gates for controlling the immune system. They are able to distinguish between disease-causing and commensal or probiotic bacteria. When the pathogenic microbes get through, the TLRs stimulate production of pro-inflammatory cytokines by activation of NF-kappaB. For example, in Crohn’s disease the TLRs are altered due to changes in the NOD2 gene. This leads to an increase in inflammation from NF-kappaB and inflammatory interleukin molecules, while blocking anti-inflammatory IL-10 and defensins.

It is believed that the constant exposure to microbes in infancy and early childhood contributes to the health and responsiveness of the adult immune system. This theory is called the “Hygiene Hypothesis.” In our culture, we don’t challenge the immune system enough: we’re too clean. We use antibacterial soaps and sponges in our obsession about microbes. As children we don’t play in the dirt; we refrigerate,
cook, and preserve our foods with chemicals, which lowers our exposure to bacterial and parasite contact. We have good sanitation, we take antibiotics, and we don’t eat fermented and cultured foods. Children who have little challenge to microbes are at risk for allergy, eczema, and asthma, which may continue throughout a lifetime. Without these challenges our immune system doesn’t develop properly.

Stress also plays a role in immune balance. Too much stress increases inflammation by modifying our gut microbiome and increases susceptibility to leaky gut.

Inflammation occurs when there is damage to cells or tissues. This is part of a normal response but can get out of control. Here are several factors that play a role.

Genetics:
Inflammatory bowel diseases, celiac disease, and arthritic diseases often have a genetic component.

Translocation of bacteria:
Even correct bacteria in the wrong place can cause problems.

Dysbiosis:
When the balance between probiotic and commensal organisms in the digestive system is overwhelmed by disease-producing microbes. Examples include bacterial, fungal, and parasitic infection.

Diet:
The Standard American Diet high in refined and poor-quality foods and low in fruits, meats, vegetables, nuts, whole grains, and seeds increases inflammatory cytokines.

Leaky gut:
No matter what the cause, having a leaky gut leads to increased inflammation.

Calprotectin and lactoferrin are proteins found in stool. They are used to help discover whether there is inflammation in the large intestine. Calprotectin and lactoferrin are often elevated in inflammatory bowel disease, postinfectious IBS, cancer in the digestive system, some GI infections, when people have caused damage from taking too many nonsteroidal anti-inflammatory medications, true food allergy, and chronic pancreatitis. When levels are high, it is a reliable marker to diagnose inflammatory bowel disease (IBD). If you have IBD, these tests can be used to monitor the
effectiveness of your chosen therapy. Stool testing is easy and is certainly less invasive than scoping of the bowels.