Digestive Tract  Permeability & Antigen Entry

Immune responses to food must be one of the most common abnormal consequences of eating. The gastrointestinal tract ( GIT) permeability to molecules, other than nutrients, is a key determinant of what happens after eating or drinking food materials. Antibody synthesis occurs at all body surfaces when antigen is presented. 

Our focus is on the interface between things ingested and the inner body space.  The boundary is the wall of the gastrointestinal tract (GIT). This boundary selects molecules for entry into the private space of self. Understanding what crosses this boundary is critical to the new understanding of food allergy and  the diseases it causes. Coombs and McLaughlin summarized the problem: 

"Food proteins in the gastrointestinal tract and their absorption into the body as antigenic molecules have immunologic significance both in

(i) initiating an allergic state and 

(ii) in the subsequent challenges whereby a variety of mechanisms they may cause some form of 'food-allergic disease."

A local GIT surface reaction to food antigens may release mast cell mediators and produce a local inflammatory swelling which in turn increases GIT permeability and permits increased entry of undigested large molecules. Unfortunately, many people ignore or suppress GIT symptoms and continue ingesting injurious substances.

The principle symptoms of GIT surface reactivity are sore throat, heartburn, abdominal pain, nausea, vomiting, diarrhea, rectal itching-burning, and distended-tender hemorrhoids. All of these symptoms disappear when the allergenic foods are eliminated.

Complex food allergy problems occur beyond the GIT but depend on GIT surveillance of food. GIT immune sensors transmit food reaction information to the entire body. We then become reactive to food antigens in other tissues. Surveillance information from GIT is distributed throughout the body by wandering lymphocytes. These cells sensitize the whole body in a discontinuous distribution. The B cells (IgA precursor cells) migrate from GIT via the draining lymph nodes; they are subsequently found in the spleen. Cells originating in GIT have a tendency to return to GIT, but some find their way throughout the lymphatic system.

Mast cells living in skin and connective tissue are also sensitized by food-inspired antibodies of the IgE and IgG classes. These "swat teams" can then react to circulating food antigens anywhere in the body. If you are immunized against an antigen presented to GIT, you can expect a response to the same antigen in any tissue. This localized distribution in different tissues of sensing, reacting immune cells is one of the reasons for the topologically distributed reactions to circulating antigens.

Increased GIT Permeability

Many factors allow allergens access to the body by interfering with GIT-surface defenses. Deficiency in the surface IgA antibody defense typically leads to delayed forms of food allergy.Without adequate IgA, large molecules are routinely absorbed through the GIT wall. We know a little about dietary factors which increase GIT permeability. Alcoholic beverages are perhaps the most important agents of increased GIT permeability. Any bacterial or viral infection which induces inflammation in the wall of GIT may increase GIT permeability. Reduced blood flow to the GIT (ischemia) increases GIT permeability and may be associated with abdominal injury, surgery, or arterial narrowing from atherosclerosis.

Water retention and swelling of the GIT wall (edema) may increase GIT permeability. During the premenstrual week, many women show increased food allergic effects as they experience generalized edema. Anti-inflammatory drugs, used to treat pain and arthritis, increase GIT permeability and may perpetuate the diseases they are used to treat. Cancer chemotherapy and radiation therapy damage the GIT and increase GIT permeability. Agent X, any molecular stressor or toxic food element, may also be involved. Deficiency of the antibody IgA promotes food allergy. This antibody is secreted on the surface of intestinal cells. The role of IgA is to trap undesirable molecules and block their entry into the absorbing surface of GIT. Deficiency of IgA would permit the entry of more allergenic macromolecules into body space via the bloodstream. Newborn infants are deficient in both serum and secretory IgA. IgA levels rise progressively in a normal child to an adult range over the first four years. IgA deficiency continues in some people as an isolated abnormality, perpetuating food allergy.

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	Managing Food Allergy
	Immunology Notes
	Alpha Nutrition Program

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