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Cross-Reaction between Gliadin and Different Food and Tissue Antigens  [PDF]
Aristo Vojdani, Igal Tarash
Food and Nutrition Sciences (FNS) , 2013, DOI: 10.4236/fns.2013.41005

A subgroup of coeliac disease patients continues to experience symptoms even on a gluten-free diet (GFD). We attempted to determine whether these symptoms could be due to either cross-contamination with gluten-containing foods or cross-reactivity between α-gliadin and non-gluten foods consumed on a GFD. We measured the reactivity of affinity-purified polyclonal and monoclonal α-gliadin 33-mer peptide antibodies against gliadin and additional food antigens commonly consumed by patients on a GFD using ELISA and dot-blot. We also examined the immune reactivity of these antibodies with various tissue antigens. We observed significant immune reactivity when these antibodies were applied to cow’s milk, milk chocolate, milk butyrophilin, whey protein, casein, yeast, oats, corn, millet, instant coffee and rice. To investigate whether there was cross-reactivity between α-gliadin antibody and different tissue antigens, we measured the degree to which this antibody bound to these antigens. The most significant binding occurred with asialoganglioside, hepatocyte, glutamic acid decarboxylase 65, adrenal 21-hydroxylase, and various neural antigens. The specificity of anti-α-gliadin binding to different food and tissue antigens was demonstrated by absorption and inhibition studies. We also observed significant cross-reactivity between α-gliadin 33-mer and various food antigens, but some of these reactions were associated with the contamination of non-gluten foods with traces of gluten. The consumption of cross-reactive foods as well as gluten-contaminated foods may be responsible for the continuing symptoms presented by a subgroup of patients with coeliac disease. The lack of response of some CD patients may also be due to antibody cross-reactivity with non-gliadin foods. These should then be treated as gluten-like peptides and should also be excluded from the diet when the GFD seems to fail.

Detection of IgE, IgG, IgA and IgM antibodies against raw and processed food antigens
Aristo Vojdani
Nutrition & Metabolism , 2009, DOI: 10.1186/1743-7075-6-22
Abstract: We developed an enzyme-linked immunosorbent assay for the measurement of IgE, IgG, IgA and IgM antibodies against raw and processed food antigens. Sera with low or high reactivity to modified food antigens were subjected to myelin basic protein, oxidized low density lipoprotein, and advanced glycation end products (AGE) such as AGE-human serum albumin and AGE-hemoglobin.Compared to raw food antigens, IgE antibodies showed a 3–8-fold increase against processed food antigens in 31% of the patients. Similarly, IgG, IgA and IgM antibodies against modified food antigens overall were found at much higher levels than antibody reactions against raw food antigens. Almost every tested serum with high levels of antibodies against modified food antigens showed very high levels of antibodies against myelin basic protein, oxidized low density lipoprotein, AGE-human serum albumin and AGE-hemoglobin.We conclude that the determination of food allergy, intolerance and sensitivity would be improved by testing IgE, IgG, IgA and IgM antibodies against both raw and processed food antigens. Antibodies against modified food antigens, by reacting with AGEs and tissue proteins, may cause perturbation in degenerative and autoimmune diseases such as diabetes, atherosclerosis, inflammation, autoimmunity, neurodegeneration and neuroautoimmunity.Adverse reactions to foods in which the pathogenesis involves an immunological response to food components are appropriately called food-hypersensitivity reactions. This term is considered to be synonymous with "food allergy." This adverse immune reaction to food proteins affects many children and adults [1]. In a study using double-blind placebo-controlled food challenge, 39% of participants showed hypersensitivity to food antigens [2].Based on clinical presentation and antibody response, immune-mediated adverse reactions to foods can be divided into immediate and delayed hypersensitivity reactions. Immediate reactions to food antigens are IgE-mediated a
The Characterization of the Repertoire of Wheat Antigens and Peptides Involved in the Humoral Immune Responses in Patients with Gluten Sensitivity and Crohn's Disease
Aristo Vojdani
ISRN Allergy , 2011, DOI: 10.5402/2011/950104
The Onset of Enhanced Intestinal Permeability and Food Sensitivity Triggered by Medication Used in Dental Procedures: A Case Report
Aristo Vojdani,Jama Lambert
Case Reports in Gastrointestinal Medicine , 2012, DOI: 10.1155/2012/265052
Abstract: Enhanced intestinal permeability and food sensitivity are two of the many proven causes of gastrointestinal disorders. This present report describes a woman with no previous gastrointestinal (GI) complaints, who underwent dental root canal, bone graft, and implant procedures. Postsurgery she experienced an allergic reaction to the combined medications. In the weeks that followed, she presented with multiple food intolerances. Four weeks after the final dental procedure, she was assessed serologically for mucosal immune function, salivary, and blood-gluten reactivity, intestinal permeability, and other food sensitivities. Compared to her test reports from two months prior to her first dental procedure, the patient’s results showed high total secretory IgA (SIgA) and elevated salivary antibodies to alpha-gliadin, indicating abnormal mucosal immunity and loss of tolerance to gluten. Her serologic assessments revealed immunoglobulin G (IgG) and IgA antibodies to a range of wheat/gluten proteins and peptides, gut bacterial endotoxins and tight junction proteins. These test results indicate gut dysbiosis, enhanced intestinal permeability, systemic gluten-reactivity, and immune response to other dietary macromolecules. The present case suggests that patients who experience severe allergic or pseudoallergic reactions to medication should be assessed and monitored for gut dysfunction. If left untreated this could lead to autoimmune reactions to self tissues.
Regulatory T Cells, a Potent Immunoregulatory Target for CAM Researchers: Modulating Tumor Immunity, Autoimmunity and Alloreactive Immunity (III)
Aristo Vojdani,Jonathan Erde
Evidence-Based Complementary and Alternative Medicine , 2006, DOI: 10.1093/ecam/nel047
Abstract: Regulatory T (Treg) cells are the major arbiter of immune responses, mediating actions through the suppression of inflammatory and destructive immune reactions. Inappropriate Treg cell frequency or functionality potentiates the pathogenesis of myriad diseases with ranging magnitudes of severity. Lack of suppressive capability hinders restraint on immune responses involved in autoimmunity and alloreactivity, while excessive suppressive capacity effectively blocks processes necessary for tumor destruction. Although the etiology of dysfunctional Treg cell populations is under debate, the ramifications, and their mechanisms, are increasingly brought to light in the medical community. Methods that compensate for aberrant immune regulation may not address the underlying complications; however, they hold promise for the alleviation of debilitating immune system-related disorders. The dominant immunoregulatory nature of Treg cells, coupled with recent mechanistic knowledge of natural immunomodulatory compounds, highlights the importance of Treg cells to practitioners and researchers of complementary and alternative medicine (CAM).
Regulatory T Cells, a Potent Immunoregulatory Target for CAM Researchers: The Ultimate Antagonist (I)
Aristo Vojdani,Jonathan Erde
Evidence-Based Complementary and Alternative Medicine , 2006, DOI: 10.1093/ecam/nek022
Abstract: Over the past decade, great interest has been given to regulatory T (Treg) cells. A vast body of evidence has shown the existence and highlighted the importance of Treg cells in the active suppression of immune system responses. This form of immunoregulation is the dominant means utilized by the immune system to reach a harmony between reciprocal response processes in order to ensure adequate host defense with minimal host detriment. Therapeutically targeting Treg cells is a direct and powerful means to manipulate the immune system to achieve beneficial effects on various disease pathologies, including allergy, autoimmunity and cancer, as well as the facilitation of organ transplantation. This powerful target for immunoregulation is of much concern to practitioners and researchers of complementary and alternative medicine because it allows a great deal of control and certainty in dealing with the prevalence of debilitating immune system-related disorders for which there has been little remedy outside of Western Medicine.
Regulatory T Cells, a Potent Immunoregulatory Target for CAM Researchers: Modulating Allergic and Infectious Disease Pathology (II)
Aristo Vojdani,Jonathan Erde
Evidence-Based Complementary and Alternative Medicine , 2006, DOI: 10.1093/ecam/nel020
Abstract: Regulatory T (Treg) cells maintain dominant control of immune responses to foreign materials and microbes. Appropriate Treg cell suppression of immune responses is essential for the maintenance of efficacious defensive responses and the limitation of collateral tissue damage due to excess inflammation. Allergy and infection are well studied and frequent afflictions in which Treg cells play an essential role. As such, they provide excellent models to communicate the significance and relevance of Treg cells to complementary and alternative medicine (CAM).
The Role of Th17 in Neuroimmune Disorders: Target for CAM Therapy. Part II
Aristo Vojdani,Jama Lambert
Evidence-Based Complementary and Alternative Medicine , 2011, DOI: 10.1093/ecam/nep063
Abstract: Decades of research went into understanding the role that Th1 autoreactive T-cells play in neuroinflammation. Here we describe another effector population, the IL-17-producing T-helper lineage (Th17), which drives the inflammatory process. Through the recruitment of inflammatory infiltration neutrophils and the activation of matrix metalloproteinases, IL-17, a cytokine secreted by Th17 cells, contributes to blood-brain barrier breakdown and the subsequent attraction of macrophages and monocytes into the nervous system. The entry of cells along with the local production of inflammatory cytokines leads to myelin and axonal damage. This activation of the inflammatory response system is induced by different pathogenic factors, such as gut bacterial endotoxins resulting in progressive neurodegeneration by Th17 cells. Through the understanding of the role of bacterial endotoxins and other pathogenic factors in the induction of autoimmune diseases by Th17 cells, CAM practitioners will be able to design CAM therapies targeting IL-17 activity. Targeted therapy can restore the integrity of the intestinal and blood-brain barriers using probiotics, N-acetyl-cysteine, α-lipoic acid, resveratrol and others for their patients with autoimmunities, in particular those with neuroinflammation and neurodegeneration. 1. Introduction In the previous article, we established the differentiation of activated T-helper cells into T-helper-17 (Th17) and the pathogenic role of interleukin-17 (IL-17) in neuroimmune disorders. Here we review the inflammatory pathophysiology of intestinal barrier permeability, which can lead to the breach of the blood-brain barrier (BBB). The tight junctions of the intestinal barrier may open due to environmental stressors, which can upset the microflora homeostasis thereby producing endotoxins that activate proinflammatory cytokine IL-1 . The upregulation of IL-1 begins a cascade of the inflammatory response system, resulting in high levels of IL-17-producing cells in various tissues. Additionally, the stressors that are capable of opening the epithelial tight junction barrier are also able to breakdown the BBB. Once inside the central nervous system, Th17 deposits IL-17 leading to CNS inflammation, which attracts additional inflammatory substances [1–6]. Neuropeptide substance P (SP), along with its high affinity receptor neurokinin-1 (NK-1), activates NF- B, a facilitator in the production of proinflammatory cytokines, and SP also reduces the production of immunoregulatory IL-10 and TGF- [7–9]. Therefore, daily environmental stressors can disrupt
The Role of Th17 in Neuroimmune Disorders: Target for CAM Therapy. Part I
Aristo Vojdani,Jama Lambert
Evidence-Based Complementary and Alternative Medicine , 2011, DOI: 10.1093/ecam/nep062
Abstract: CD4+ effector cells, based on cytokine production, nuclear receptors and signaling pathways, have been categorized into four subsets. T-helper-1 cells produce IFN-γ, TNF-β, lymphotoxin and IL-10; T-helper-2 cells produce IL-4, IL-5, IL-10, IL-13, IL-21 and IL-31; T-helper-3, or regulatory T-cells, produce IL-10, TGF-β and IL-35; and the recently discovered T-helper-17 cell produces IL-17, IL-17A, IL-17F, IL-21, IL-26 and CCL20. By producing IL-17 and other signaling molecules, Th17 contributes to the pathogenesis of multiple autoimmune diseases including allergic inflammation, rheumatoid arthritis, autoimmune gastritis, inflammatory bowel disease, psoriasis and multiple sclerosis. In this article, we review the differential regulation of inflammation in different tissues with a major emphasis on enhancement of neuroinflammation by local production of IL-17 in the brain. By understanding the role of pathogenic factors in the induction of autoimmune diseases by Th17 cells, CAM practitioners will be able to design CAM therapies targeting Th17 and associated cytokine activities and signaling pathways to repair the intestinal and blood-brain barriers for their patients with autoimmunities, in particular, those with neuroinflammation and neurodegeneration. 1. Introduction For more than 30 years T-helper (Th) cells have been divided by immunologists into two functional subsets: T-helper-1 (Th1) and T-helper-2 (Th2). Th1 and Th2 subsets are characterized by a distinct activity of transcription factor and pattern of cytokine-secretion phenotype [1, 2]. This differentiation of CD4+ T-cells toward Th1, Th2 and other subsets depends on an appropriate signal through the TCR and generated cytokine milieu is an important factor that influences CD4 cell lineage commitment. For example, interleukin (IL)-12 activates STAT4 and drives na?ve CD4+ T cells to become Th1 cells that produce interferon-gamma (INF- ). These signals from IL-12 and IFN- by acting through STAT4 and STAT1, increase the expression of the transcription factor called T-bet, which promotes further production of IFN- and commitment to the Th1 cell lineage. Th1 cells classically produce IFN- , tumor necrosis factor-beta (TNF- ) and interleukin-10 (IL-10), and mediate cellular immune responses against tumor cells, intracellular viruses and bacteria through activation of macrophages and cytotoxic T-cells. In addition, Th1 cells drive cell-mediated response leading to tissue damage and drive humoral immune responses in certain immunoglobulin subclasses termed Ig2a. Innate immune cells, by signals through
Differentiation between Celiac Disease, Nonceliac Gluten Sensitivity, and Their Overlapping with Crohn’s Disease: A Case Series
Aristo Vojdani,David Perlmutter
Case Reports in Immunology , 2013, DOI: 10.1155/2013/248482
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