Infections and celiac disease

Abstract

Celiac disease (CD) is a chronic autoimmune disease with a global prevalence of 1%. It is known to develop after ingestion of gluten-rich foods in genetically susceptible individuals. Variants in HLA-DQA1 and HLA-DQB1 genes encoding the alpha and beta chains of DQ2 and DQ8 proteins, are seen in more than 90% of patients. Genetic predisposition is necessary but not sufficient to develop CD, as only low percent of genetically predisposed individuals develop CD. Typical CD manifests with diarrhea alongside findings of malabsorption. Gluten is composed of unusual repetitive sequences of amino acids which make it difficult to fully digest the large peptides formed. By crossing intestinal lamina propria these peptides activate both innate and adaptive immune system causing an inflammatory cascade. Environmental factors play an important role in the pathogenesis of CD. An increased number of respiratory infections during the first 18 months of life seems to increase the risk of developing CD in later years. Additionally, there are rising evidence on the involvement of EBV and Enteroviruses in the pathogenesis of CD. Recently, COVID-19 was associated with CD. Moreover, gastrointestinal infections have been listed as a risk factor for CD. Among other suggested mechanisms, molecular mimicry and bystander activation are the leading theories. In our current chapter, we aimed to elaborate on the correlation between infections and the development of CD.