Advances in coeliac disease

Lundin, Knut E.A.; Sollid, Ludvig M.

doi:10.1097/mog.0000000000000041

Cited by 57 publications

(41 citation statements)

References 109 publications

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“…Celiac disease is an inflammatory enteropathy caused by gluten from wheat and other cereals in genetically predisposed individuals. 103 A link between the HSP70-2 gene and celiac disease was first reported in 1993. 104 Then, the C allele of the HSP70-1 gene was reported to be higher in Spanish celiac patients and was therefore considered an additional factor in celiac disease susceptibility.…”

Section: Inflammatory Bowel Disease and Celiac Diseasementioning

confidence: 99%

Gut epithelial inducible heat-shock proteins and their modulation by diet and the microbiota

Arnal

Lallès

2016

Nutr Rev

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Section: Inflammatory Bowel Disease and Celiac Diseasementioning

confidence: 99%

Gut epithelial inducible heat-shock proteins and their modulation by diet and the microbiota

Arnal

Lallès

2016

Nutr Rev

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“…Untreated CD is characterized by autoantibodies to tissue transglutaminase (TG2), an (intestinal) enzyme that binds and modifies gluten peptides, resulting in their improved binding to HLA-DQ2 or HLA-DQ8, the major genetic predisposition for CD, followed by activation and expansion of destructive Th1 T cells in the gut (1). Apart from the established roles of gluten, HLA-DQ2/HLA-DQ8, and TG2, environmental factors such as viral and microbial infections and perhaps feeding practices have also been suggested to contribute to CD pathogenesis (2)(3)(4)(5)(6).…”

mentioning

confidence: 99%

Salivary Gluten Degradation and Oral Microbial Profiles in Healthy Individuals and Celiac Disease Patients

Tian

Faller²,

Leffler

et al. 2017

Appl Environ Microbiol

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Celiac disease (CD) is a chronic immune-mediated enteropathy induced by dietary gluten in genetically predisposed individuals. Saliva harbors the second highest bacterial load of the gastrointestinal (GI) tract after the colon. We hypothesized that enzymes produced by oral bacteria may be involved in gluten processing in the intestine and susceptibility to celiac disease. The aim of this study was to investigate salivary enzymatic activities and oral microbial profiles in healthy subjects versus patients with classical and refractory CD. Stimulated whole saliva was collected from patients with CD in remission (n ϭ 21) and refractory CD (RCD; n ϭ 8) and was compared to healthy controls (HC; n ϭ 20) and subjects with functional GI complaints (n ϭ 12). Salivary gluten-degrading activities were monitored with the tripeptide substrate Z-Tyr-Pro-Gln-pNA and the ␣-gliadin-derived immunogenic 33-mer peptide. The oral microbiome was profiled by 16S rRNA-based MiSeq analysis. Salivary glutenase activities were higher in CD patients compared to controls, both before and after normalization for protein concentration or bacterial load. The oral microbiomes of CD and RCD patients showed significant differences from that of healthy subjects, e.g., higher salivary levels of lactobacilli (P Ͻ 0.05), which may partly explain the observed higher gluten-degrading activities. While the pathophysiological link between the oral and gut microbiomes in CD needs further exploration, the presented data suggest that oral microbe-derived enzyme activities are elevated in subjects with CD, which may impact gluten processing and the presentation of immunogenic gluten epitopes to the immune system in the small intestine.IMPORTANCE Ingested gluten proteins are the triggers of intestinal inflammation in celiac disease (CD). Certain immunogenic gluten domains are resistant to intestinal proteases but can be hydrolyzed by oral microbial enzymes. Very little is known about the endogenous proteolytic processing of gluten proteins in the oral cavity. Given that this occurs prior to gluten reaching the small intestine, such enzymes are likely to contribute to the composition of the gluten digest that ultimately reaches the small intestine and causes CD. We demonstrated that endogenous salivary protease activities are incomplete, likely liberating peptides from larger gluten proteins. The potentially responsible microbes were identified. The study included refractory CD patients, who have been studied less with regard to CD pathogenesis.

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“…Lundin at al., recently designed current challenges in celiac disease as necessity of better case finding, distinguishing celiac disease from other gluten-sensitive conditions, better care and balanced use of resources [35]. Researchers have already described susceptibility loci and a number of genes associated with celiac disease with a well-known close association with the HLA-DQ2 and/or DQ8 genes.…”

Section: Discussionmentioning

confidence: 99%

Genetic Aspects of Celiac Disease in Association with Pancreatic Tumors

Procházka¹

2016

IJCD

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Celiac disease stands out as a major health problem with a frequent association with many other disorders. Studies show an increased risk of developing pancreatitis and after that pancreatic cancer in patients with celiac disease. A frequent occurrence and a remarkably close association with the HLA-DQ2 and/or DQ8 gene loci represent main genetic characteristic of celiac disease. A particular association was found with chromosome 15q26 and 6q21-22. On the other hand pancreatic tumors are known for associations with CTNNB1, VHL, CDKN2A, KRAS, TP53, RNF43, SMAD4, GNAS, PRSS1, ATM, BRCA1, BRCA2, PALB2, STK11 and hereditary non-polyposis colorectal cancer syndrome genes. Recent genetic mapping suggests that a large field of opportunities exists for better understanding of both diseases.

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Advances in coeliac disease

Cited by 57 publications

References 109 publications

Gut epithelial inducible heat-shock proteins and their modulation by diet and the microbiota

Gut epithelial inducible heat-shock proteins and their modulation by diet and the microbiota

Salivary Gluten Degradation and Oral Microbial Profiles in Healthy Individuals and Celiac Disease Patients

Genetic Aspects of Celiac Disease in Association with Pancreatic Tumors

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