The molecular basis of coeliac disease

Hourigan, Christopher S.

doi:10.1007/s10238-006-0095-6

Cited by 22 publications

(13 citation statements)

References 43 publications

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“…The presence of heterodimers DQA1*03-DQB1*0302, DQA*05, or DQB1*02, on the other hand, was detected in fewer cases (Hourigan, 2006). Previous studies investigating the pathogenesis of CD have reported that oxidative stress plays an important role in the development of the disease (Cheeseman and Slater, 1993;Preedy et al, 1998).…”

Section: Introductionmentioning

confidence: 92%

Evaluation of glutathione peroxidase and superoxide dismutase enzyme polymorphisms in celiac disease patients

et al. 2014

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ABSTRACT. Celiac disease (CD) is a multifactorial, inflammatory small bowel disorder characterized by nutrient malabsorption resulting from mucosal damage, the latter induced by cereal products like barley, oat, and wheat. Oxidative stress has previously been reported to play an important role in the pathogenesis of CD. In the present study, we aimed to evaluate the frequency of polymorphisms that affects the structure of the enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), with levels being dependent on the amount of oxidative stress and whether or not there is an association with the mutations DQA1*0501, DQB1*0201, and DRB1*04 that are frequently reported for CD. SOD and GSH-Px polymorphisms were investigated by realtime quantitative polymerase chain reaction in 265 cases. Of the 117 cases that had at least one of DQA1*0501, DQB1*0201, or DRB1*04, 98 (83.75%) also had SOD enzyme polymorphisms and 68 (58.12%) also had GSH-Px polymorphisms. In conclusion, although the etiology of CD is not yet entirely clear, many mechanisms have been suggested. This study supports the notion that SOD and GSH-Px polymorphisms are involved in CD development, even though our findings were not Antioxidant enzyme polymorphisms in celiac disease statistically significant, and, furthermore, are influenced at various levels. SOD polymorphisms and activities were more frequently identified than those of GSH-Px.

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Section: Introductionmentioning

confidence: 92%

Evaluation of glutathione peroxidase and superoxide dismutase enzyme polymorphisms in celiac disease patients

et al. 2014

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“…Furthermore, a pathogenetic function of enterocytes in CD has been suggested; morphological studies using immunofluorescence microscopy showed that increased amounts of gliadin peptides were present in intracellular compartments of enterocytes of CD patients in remission compared with control enterocytes (Friis et al 1992;Zimmer et al 1998). Gluten peptides that have passed the enterocyte layer and arrived at the lamina propria are able to trigger two immunological pathways; one is the adaptive immune response involving antigen presenting cells (APC), HLA-DQ2 or HLA-DQ8 heterodimers and CD4 + T-cells in the lamina propria, and the other presents the innate immune response thought to be a rapid effect on the epithelium (recently reviewed by Ciccocioppo et al 2005;Londei et al 2005;Hourigan 2006;Kagnoff 2007).…”

Section: Digestion and Epithelial Passagementioning

confidence: 99%

The Biochemical Basis of Celiac Disease

2008

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Cereal Chem. 85(1):1-13Celiac disease (CD) is an inflammatory disorder of the upper small intestine triggered by the ingestion of wheat, rye, barley, and possibly oat products. The clinical feature of CD is characterized by a flat intestinal mucosa with the absence of normal villi, resulting in a generalized malabsorption of nutrients. The prevalence of CD among Caucasians is now thought to be in a range of 1:100-300. There is a strong genetic association with human leukocyte antigens (HLA-)DQ2 and DQ8 and currently unknown non-HLA genes. During the last decade, intense biochemical studies have contributed to substantial progress in understanding the general principles that determine the pathogenesis of CD. The precipitating factors of toxic cereals are the storage proteins, termed gluten in the field of CD (gliadins and glutenins of wheat, secalins of rye, and hordeins of barley). There is still disagreement about the toxicity of oat avenins. The structural features unique to all CD toxic proteins are sequence domains rich in Gln and Pro. The high Pro content renders these proteins resistant to complete proteolytic digestion by gastrointestinal enzymes. Consequently, large Pro-and Gln-rich peptides are cumulated in the small intestine and reach the subepithelial lymphatic tissue. Depending on the amino acid sequences, these peptides can induce two different immune responses. The rapid innate response is characterized by the secretion of the cytokine interleukin-15 and the massive increase of intraepithelial lymphocytes. The slower adaptive response includes the binding of gluten peptides (native or partially deamidated by tissue transglutaminase) to HLA-DQ2 or -DQ8 of antigen presenting cells and the subsequent stimulation of T-cells accompanied by the release of proinflammatory cytokines such as interferon-γ and the activation of matrix metalloproteinases. Both immune responses result in mucosal destruction and epithelial apoptosis. Additionally, stimulated T-cells activate B-cells that produce serum IgA and IgG antibodies against gluten proteins (antigen) and tissue transglutaminase (autoantigen). These antibodies can be used for noninvasive screening tests to diagnose CD. The current essential therapy of CD is a strict lifelong adherence to gluten-free diet. Dietetic gluten-free foods produced for CD patients underlie the regulations of the Codex Alimentarius Standard for Gluten-Free Foods. The "Draft Revised Codex Standard" edited in March 2006 proposes a maximum level of 20 mg of gluten/kg for naturally gluten-free foods (e.g., based on rice or corn flour) and 200 mg/kg for foods rendered gluten-free (e.g., wheat starch). Numerous analytical methods for gluten determination have been developed, mostly based on immunochemical assays, mass spectrometry, or polymerase chain reaction. So far, only two enzyme-linked immunosorbent assays have been successfully ring-tested and are commercially available. During the last decade, future strategies for prevention and treatment of CD have been proposed. They are based...

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“…This causes the activation of T cells, which leads to a cascade of intracellular reactions, damaging intestinal epithelium and causing various degrees of villous atrophy (Marsh or Schmerling scale). At the same time, the deaminated gluten molecule being a potent antigen induces the production of antibodies against tTG, endomysium (EMA), gliadin and reticulum [1].…”

Section: Introductionmentioning

confidence: 99%

Endocrine disorders and coeliac disease

Waszczuk¹,

Jawny²

2011

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Coeliac disease (coeliac sprue, gluten-related enteropathy) is both digestive intolerance and an autoimmune disorder. It is a multifactorial disorder in which genetic, immune, environmental and metabolic factors seem to be most important in its pathogenesis. Because of the diversity of clinical symptoms and more frequent occurrence of this disease than was previously assumed, coeliac disease should be taken into consideration in general practice and specialty clinics (especially endocrinology). The aim of this review article is to present and discuss the associated endocrine disorders that are often the first symptoms of coeliac disease or can suggest its coexistence. Therefore, fast diagnosis and introduction of a glutenfree diet can completely withdraw some of the endocrine disorders, support their treatment and prevent the development of severe complications. StreszczenieChoroba trzewna (coeliac disease -CD) to zapalna enteropatia jelita cienkiego. Objawy schorzenia pojawiają się u osób predysponowanych genetyczne, jednak ważną rolę odgrywają również czynniki immunologiczne, środowiskowe i metaboliczne. Ze względu na częste występowanie i różne postaci kliniczne CD powinno się brać pod uwagę możliwość jej występowania w ośrodkach podstawowej i specjalistycznej opieki zdrowotnej, zwłaszcza endokrynologicznych. Autorzy pracy zwracają uwagę na schorzenia endokrynologiczne, któ-re częściej współistnieją z CD, oraz na problem poszukiwania tej choroby wśród pacjentów endokrynologicznych. Ustalenie właściwego rozpoznania i włączenie diety bezglutenowej uchroni pacjentów przed wystąpieniem kolejnych objawów i zapobiegnie ciężkim powikłaniom.

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The molecular basis of coeliac disease

Cited by 22 publications

References 43 publications

Evaluation of glutathione peroxidase and superoxide dismutase enzyme polymorphisms in celiac disease patients

Evaluation of glutathione peroxidase and superoxide dismutase enzyme polymorphisms in celiac disease patients

The Biochemical Basis of Celiac Disease

Endocrine disorders and coeliac disease

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