Abstract
The ingestion of wheat gliadin (alcohol-soluble proteins, an integral part of wheat gluten) and related proteins induce, in genetically predisposed individuals, celiac disease (CD), which is characterized by immune-mediated impairment of the small intestinal mucosa. The lifelong omission of gluten and related grain proteins, i.e., a gluten-free diet (GFD), is at present the only therapy for CD. Although a GFD usually reduces CD symptoms, it does not entirely restore the small intestinal mucosa to a fully healthy state. Recently, the participation of microbial components in pathogenetic mechanisms of celiac disease was suggested. The present review provides information on infectious diseases associated with CD and the putative role of infections in CD development. Moreover, the involvement of the microbiota as a factor contributing to pathological changes in the intestine is discussed. Attention is paid to the mechanisms by which microbes and their components affect mucosal immunity, including tolerance to food antigens. Modulation of microbiota composition and function and the potential beneficial effects of probiotics in celiac disease are discussed.
Highlights
Laboratory of Cellular and Molecular Immunology, Institute of Microbiology of the Czech Academy of Department of Internal Medicine, University Hospital Královské Vinohrady and Third Faculty of Medicine, First Faculty of Medicine, Charles University, Kateřinská 1660/32, 121 08 Prague, Czech Republic
Mucosal infections may contribute to the impairment of immune tolerance to gluten, leading to tissue damage in celiac disease (CD) patients [46]. Infections, mainly those induced by Clostridium difficile, Helicobacter pylori, and Streptococcus pneumoniae (Pneumococcus), are frequently associated with CD
Analyses of bacterialderived small RNA could help elucidate the complicated relationship between microbiota and host relative to the pathogenesis of CD [103]
Summary
The ingestion of wheat gliadin (the alcohol-soluble part of wheat grain storage proteins, i.e., gluten) and phylogenetically related cereal proteins (secalin from rye, hordein from barley, and avenin from oat) induces celiac disease (CD) in genetically susceptible individuals bearing the human leukocyte antigens HLA-DQ2 (alleles DQA1*0501 and DQB1*0201) and HLA-DQ8 (DQA1*0301 and DQB1*0302) haplotypes [1,2,3,4]. Life-long adherence to a gluten-free diet (GFD) is the sole rational therapy for CD, with the goal of healing pathological changes in the gut mucosa and suppressing the production of antibodies and autoantibodies [3,5,6,7,8,9]. Microorganisms 2021, 9, 547 gluten-free diet (GFD) is the sole rational therapy for CD, with the goal of healing pathological changes in the gut mucosa and suppressing the production of antibodies and autoantibodies [3,5,6,7,8,9]. Antibodies against gliadin and autoantibodies against remodeling of small gut mucosa of celiac patients. Decreased in CD patients [32,34,35,36]
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