Patricia Laughlin
Celiac Disease (CD) is a prevalent systemic condition arising from an aberrant immune reaction to gluten consumption, primarily affecting the small intestine. In individuals with a genetic predisposition, CD can be incited by external factors, such as viral infections and disruptions in the gut microbiota, known as dysbiosis. The gut microbiome plays a crucial role in regulating the immune system, and recent discoveries suggest that alterations in the gut microbiome might contribute to various chronic immune disorders, including CD, although the precise mechanisms are still under investigation. Certain bacteria in the gut exhibit epitopes that resemble gliadin, potentially intensifying the host's immune response. Additionally, some bacteria, like Pseudomonas aeruginosa, may collaborate with gluten to initiate and exacerbate intestinal inflammation. The microbiota might also directly influence antigen formation by generating immunogenic or tolerogenic gluten peptides. Furthermore, it could impact intestinal permeability by releasing zonulin, a protein associated with gut barrier function. Based on existing research, changes in the gut microbiome linked to CD typically involve a reduction in beneficial bacteria, including certain antiinflammatory Bifidobacterium species. However, it's worth noting that there is still some debate in this area, as certain studies have not detected significant distinctions in the gut microbiomes of individuals with and without CD. Obtaining a more comprehensive understanding of how the gut microbiome contributes to the development of CD would be highly advantageous for improving both preventive measures and treatment strategies, particularly in cases that are complex or resistant to conventional therapies