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Celiac disease
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Celiac disease is a chronic, T-cell–mediated, inflammatory disorder of the small intestine resulting from an inappropriate immune response to gluten. Gluten is a complex of proteins present in wheat, barley, and rye. Wheat gluten proteins consist of α-, γ-, and ω-gliadins as well as high and low molecular weight glutenin subcomponents. Both gliadin and glutenin proteins can induce the disease, which is treated with a lifelong gluten exclusion diet. The mucosal pathology associated with celiac disease is localized to the proximal small intestine and is characterized by villus atrophy and prominent infiltration of leukocytes into the epithelium and lamina propria. The mucosal absorptive surface is reduced as a consequence of villus atrophy, leading to malabsorption that may result in anemia and steatorrhea. Additional symptoms, including fatigue, infertility, neurologic manifestations, and enamel defects, may not indicate an intestinal disease, and some patients have few or even no symptoms. The eclectic nature of the symptoms is a challenge to clinicians, and consequently, many patients are not diagnosed or experience long delays before diagnosis.
Major Histocompatibility Complex and Autoimmune Disease
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Ursula Holzer, Gerald T. Nepom
Celiac disease is another chronic HLA-associated disease with multifactorial etiologies where genetic and environmental components are involved. The disease is an inflammatory disorder in which the mucosa of the small intestine is damaged in response to ingestion of gliaden proteins contained in wheat gluten. The primary HLA association in patients is with either the DRB1*0301-DQA1*0501 -DQB1*0201 haplotype or in heterozygotes with the same HLA-DQ alleles, encoded in trans-, forming a heterodimer encoded by the DQ beta chain from the DRB1*0701-DQA1*0201-DQB1*0201 haplotype and the DQ alpha chain from the DRB1*1101-DQA1*0501-DQB1*0201 haplotype.66 Dermatitis herpetiformis, a blistering skin disease characterized by granular IgA deposits in the papillary dermis is associated with similar HLA polymorphisms: HLA DRB1*0301 and DQA1*0501-DQB1*02.66-68 The association with the DRB markers in both disorders is probably secondary to linkage disequilibrium with the DQ alleles mentioned above in Caucasians.
Treating the Dysmetabolism Underlying Osteoporosis
Published in Kohlstadt Ingrid, Cintron Kenneth, Metabolic Therapies in Orthopedics, Second Edition, 2018
Gluten-sensitive enteropathy (Celiac disease). Celiac disease is an autoimmune disorder of varying severity characterized by small bowel enteropathy resulting from exposure to wheat gluten in genetically susceptible individuals and is frequently diagnosed in patient s presenting with osteoporosis [36]. Auto-antibodies to OPG have been identified in subjects with celiac disease [93].
Lack of Efficacy of the Neutropenic Diet in Decreasing Infections among Cancer Patients: A Systematic Review
Published in Nutrition and Cancer, 2020
Venkataraghavan Ramamoorthy, Muni Rubens, Sandeep Appunni, Anshul Saxena, Peter McGranaghan, Emir Veledar, Ana Viamonte-Ros, Nancy Shehadeh, Adeel Kaiser, Rupesh Kotecha
An open question is whether preventing leaky gut syndrome to limit microbial transit may be more effective than reducing the overall microbial content of food. This question has merit since gut permeability remains a hallmark pathway for bacteremia (5), with most cases of sepsis arising from commensal organisms already on or within the body (10). Preclinical data suggests that increasing dietary fat may enhance the barrier properties of gastrointestinal mucus (35). Butyrate, a short-chain fatty acid, promotes colonocyte proliferation and healing through growth factor induction (36). Butyrate is a major energy source for enterocytes and maintains epithelial integrity for antimicrobial defense through epigenetic effects on DNA methylation and histone acetylation (37). Phase III data in colitis suggests that phosphatidylcholine, a major constituent of biological membranes, and readily available in egg yolks, improves intestinal injury and may be beneficial in neutropenia (38). Conversely, limitation of anti-nutrients that enhance intestinal permeability may also be advantageous for neutropenic patients. Gliadin, the main fraction of wheat gluten responsible for the intestinal damage in celiac disease, increases gut permeability to macromolecules (39). This impact on mucosal integrity is observable irrespective of the presence of autoimmunity.
Deciphering crucial genes in coeliac disease by bioinformatics analysis
Published in Autoimmunity, 2020
Effat Noori, Bahram Kazemi, Mojgan Bandehpour, Hakimeh Zali, Bahman Khalesi, Saeed Khalili
Coeliac disease (CD) is a chronic autoimmune disorder with a high genetic predisposition that is triggered by the ingestion of wheat gluten. It is a multifactorial disease with a worldwide prevalence of 1% that is induced by genetic and environmental factors. CD exhibits a wide spectrum of clinical representations that can involve almost any organ of the body. CD patients mainly suffer from intestinal abnormalities [1–3]. Epidemiological studies have shown that the CD is widespread and increasing, especially in Western countries and the US [4]. Differences in the prevalence CD are reported between countries; for instance, in Western Sahara, the CD prevalence is 5.6% while in Burkina Faso, no CD cases are recorded [5]. Changes in the consumption pattern increased processing of the food, and expanded consumption of gluten-containing foods are thought to be the reason behind the increased incidences of CD [6]. CD is characterized by severe autoimmune responses [1]. Both innate and adaptive immune systems are involved in the pathogenesis of CD [7]. Undesirable immunological reactions could cause inflammation and villous atrophy of the small intestine that could result in malabsorption of vitamins and nutrients [3].
Going gluten free in non-celiac autoimmune diseases: the missing ingredient
Published in Expert Review of Clinical Immunology, 2018
Aaron Lerner, Ajay Ramesh, Torsten Matthias
Wheat is the most important source of carbohydrate in the Western world with a constant increase in sales also in Eastern societies. Since gluten comprises 80% of the contemporary wheat proteins and is also heavily used as a food additive in the processed food industries, no doubt that its consumption is surging [1], in parallel to the increased prevalence in multiple autoimmune diseases (ADs), at list in recent decades [2]. Interestingly, an 8-fold increase in the wheat gluten content was observed, since it discovery around 15,000 years ago, in the Middle East Fertile Crescent. Owing to its evolutionary increased wheat content, its augmented immunogenicity and toxicity, and its multiple detrimental effects, gluten might be associated to some modern chronic disease development [1–3]. Being an ideal substrate for ex- and in-vivo enzymatic post translational modification of proteins, thus inducing physico-chemical and 3-dimensional changes, turning naive gluten to a neo-epitope peptide, the transformed gluten becomes a prime candidate to drive autoimunogenesis [1,3–6]. In fact, despite its popular use in food, gluten appears to have multiple side effects: increases intestinal permeability, changes composition and diversity of the microbiome/dysbiome ratio, increases oxidative stress, and changes epigenetic processes. Gluten was shown to be immunogenic, cytotoxic, proapoptotic, and proinflammatory. At the cellular level, it decreases cell differentiation and viability [3].