Why is coeliac disease endemic in the people of the Sahara?

Catassi, Carlo; Rätsch, I M; Gandolfi, Lenora; Pratesi, Riccardo; Fabiani, Elisabetta; Asmar, Ramzi El; Frijia, M; Bearzi, Italo; Vizzoni, L

doi:10.1016/s0140-6736(99)02609-4

Cited by 234 publications

(145 citation statements)

References 5 publications

Supporting

Mentioning

127

Contrasting

Unclassified

Order By: Relevance

“…The key role of gluten in the pathogenesis of CD has been established through epidemiological studies and the observation that CD patients enter remission when they adhere to a gluten-free diet. Saharawi 21 and Latin American 22 populations experienced an increased prevalence of CD after changing their low-gluten diets to gluten-enriched diets. We thus hypothesised that the elimination of gluten from the diet would allow for newborns to acquire intolerance against gliadin-derived peptides that exacerbate the immune responses against orally introduced gliadin and trigger enteropathy.…”

Section: Discussionmentioning

confidence: 99%

Gluten induces coeliac-like disease in sensitised mice involving IgA, CD71 and transglutaminase 2 interactions that are prevented by probiotics

Papista

Gerakopoulos

Kourelis

et al. 2012

Laboratory Investigation

View full text Add to dashboard Cite

Coeliac disease (CD) is a malabsorptive enteropathy resulting from intolerance to gluten. Environmental factors and the microbiota are suggested to have critical roles in the onset of CD. The CD71 IgA receptor on epithelial cells is responsible for abnormal retrotranscytosis of IgA-gluten peptide complexes from the intestinal lumen into the lamina propria, inducing intestinal inflammation. However, understanding the role of gluten in the CD physiopathology has been hindered by the absence of relevant animal models. Here, we generated a mouse model for CD to study the factors controlling its pathogenesis as well as to investigate the influence of oral delivery of probiotics on disease development. Gluten sensitivity was established by feeding three generations of BALB/c mice a gluten-free diet (GÀ) followed by gluten challenge (G þ ) for 30 days. The G þ mice developed villous atrophy, crypt hyperplasia and infiltration of T cells and macrophages in the small intestine. Inflammation was associated with an overexpression of CD71 on the apical side of enterocytes and an increase of plasma cells producing IgA, which colocalised with the CD71. Moreover, IgA colocalised with the transglutaminase 2 (TG2), the production of which was increased in the lamina propria of G þ mice. These mice displayed increased production of cyclooxygenase-2 (COX-2), pro-inflammatory cytokines and IL-15, as well as anti-gliadin and anti-TG2 autoantibodies. The commensal flora-isolated presumptive probiotic Saccharomyces boulardii KK1 strain hydrolysed the 28-kDa a-gliadin fraction, and its oral delivery in G þ mice improved enteropathy development in association with decrease of epithelial cell CD71 expression and local cytokine production. In conclusion, the G þ BALB/c mouse represents a new mouse model for human CD based on histopathological features and expression of common biomarkers. The selected probiotic treatment reversing disease development will allow the study of the role of probiotics as a new therapeutic approach of CD.

show abstract

Section: Discussionmentioning

confidence: 99%

Gluten induces coeliac-like disease in sensitised mice involving IgA, CD71 and transglutaminase 2 interactions that are prevented by probiotics

Papista

Gerakopoulos

Kourelis

et al. 2012

Laboratory Investigation

View full text Add to dashboard Cite

show abstract

“…The current prevalence of CD in the Western countries is estimated at between 1:80 and 1:100 (16,(20)(21)(22)(23)(24). Identification of anti-tTG and EMA antibodies as a marker for CD has caused AGA to lose the diagnostic role they had held since the early 80s (25).…”

Section: Discussionmentioning

confidence: 99%

Diagnostic efficacy of the ELISA test for the detection of deamidated anti‐gliadin peptide antibodies in the diagnosis and monitoring of celiac disease

Tonutti

Visentini

Picierno

et al. 2009

Clinical Laboratory Analysis

View full text Add to dashboard Cite

Background and Aim: We evaluated the diagnostic performance of an ELISA test for anti-gliadin IgA and IgG antibodies, which uses synthetic deamidated gliadin peptides (anti-gliadin antibodies, AGAs) as coating; the results were compared with a test that uses extracted gliadin (AGAe). Methods: The study was conducted on the sera of 144 patients suffering from celiac disease (CD), including 20 patients with IgA deficiency and 9 who were following a gluten-free diet (GFD), and 129 controls. Results: In the 115 CD patients (without IgA deficiency), the sensitivity of AGAe IgA and IgG was 32.2 and 60.9%, whereas that of AGAs IgA and IgG was 59.1 and 72.2%. The specificity for AGAe IgA and IgG, and AGAs IgA and IgG was 93.8 and 89.9%, and 96.9% and 99.2%, respectively. Of the 20 patients with CD and IgA deficiency, 7 tested positive for AGAe IgG and 14 for AGAs IgG. The test using deamidated gliadin peptides performed better in terms of sensitivity and specificity than the AGA tests with extracted antigen. Conclusions: The very high specificity of the AGAs IgG test (99.2%) also suggests that patients who test positive with this assay require a thorough followup, even if the anti-tissue transglutaminase antibodies (anti-tTG) and anti-endomysial autoantibodies (EMA) assays are negative.

show abstract

“…The amazingly high CD prevalence in children of the Sahara (1 in 18) can be partially explained by the high amount of cereal (couscous) in the diet and by the particular genetic background of this population (i.e., high prevalence of HLA-DQ2/DQ8). 24 CD can manifest in any age group, from infants to the elderly. Retrospective analysis of clinical data shows that most adult celiacs had no sign of the disease during their childhood, thereby confirming that CD can develop in adulthood.…”

Section: Introductionmentioning

confidence: 99%

Celiac disease: diagnostic criteria in progress

2011

View full text Add to dashboard Cite

Until a few years ago, celiac disease (CD) was thought to be a rare food intolerance that was confined to childhood and characterized by severe malabsorption and flat intestinal mucosa. Currently, CD is regarded as an autoimmune disorder that is common in the general population (affecting 1 in 100 individuals), with possible onset at any age and with many possible presentations. The identification of CD is challenging because it can begin not only with diarrhea and weight loss but also with atypical gastrointestinal (constipation and recurrent abdominal pain) and extra-intestinal symptoms (anemia, raised transaminases, osteoporosis, recurrent miscarriages, aphthous stomatitis and associated autoimmune disorders), or it could be completely symptomless. Over the last 20 years, the diagnostic accuracy of serology for CD has progressively increased with the development of highly reliable tests, such as the detection of IgA tissue transglutaminase and antiendomysial and IgG antideamidated gliadin peptide antibodies. The routine use of antibody markers has allowed researchers to discover a very high number of 'borderline' cases, characterized by positive serology and mild intestinal lesions or normal small intestine architecture, which can be classified as potential CD. Therefore, it is evident that the 'old celiac disease' with flat mucosa is only a part of the spectrum of CD. It is possible that serology could identify CD in its early stages, before the appearance of severe intestinal damage. In cases with a positive serology but with mild or absent intestinal lesions, the detection of HLA-DQ2 and HLA-DQ8 can help reinforce or exclude the diagnosis of gluten sensitivity.

show abstract

Why is coeliac disease endemic in the people of the Sahara?

Cited by 234 publications

References 5 publications

Gluten induces coeliac-like disease in sensitised mice involving IgA, CD71 and transglutaminase 2 interactions that are prevented by probiotics

Gluten induces coeliac-like disease in sensitised mice involving IgA, CD71 and transglutaminase 2 interactions that are prevented by probiotics

Diagnostic efficacy of the ELISA test for the detection of deamidated anti‐gliadin peptide antibodies in the diagnosis and monitoring of celiac disease

Celiac disease: diagnostic criteria in progress

Contact Info

Product

Resources

About