Role of the gut microbiota in the pathogenesis of coeliac disease and potential therapeutic implications

Abstract

Purpose Although genetic predisposition and exposure to dietary gluten are considered necessary triggers for the development of coeliac disease, alterations in the gut microbial composition may also contribute towards the pathogenesis of coeliac disease. This review aims to provide an overview of the available data on the potential mechanisms through which the gut microbiota plays a role in the causation of coeliac disease and to discuss the potential therapeutic strategies that could diminish the consequences of microbial dysbiosis. Method A search of the literature was performed using the PubMed, Embase, and JSTOR databases; relevant articles were included. Results Recent studies in patients with coeliac disease have reported an increase in the relative amounts of gram negative bacterial genera such as Bacteroides, Prevotella, and Escherichia, and reduced amounts of protective anti-inflammatory bacteria such as Bifidobacteria and Lactobacilli. Dysbiotic microbiota may lead to a dysregulated immune response that may contribute to the pathogenesis of coeliac disease. In infancy, antibiotic use and certain infant feeding practices may lead to alterations in the developing gut microbiota to influence the immune maturation process and predispose to coeliac disease. Conclusion The induction of the intestinal immune system and gluten intolerance may be influenced by the relative abundance of certain microbiota. Factors such as infant feeding practices, diet, antibiotics, and infections, may be involved in the development of coeliac disease due to their influence on gut microbial composition. The efficacy of potential modulators of the gut microbiota such as probiotics, prebiotics, and fecal microbial transplant as adjunctive treatments to gluten-free diet in coeliac disease is unproven and requires further investigation.

The role of the microbiome in gastrointestinal inflammation

“…Coeliac disease, prevalent in 1–2% of the global population, is an immune-mediated inflammatory disorder that primarily affects the small intestine and is initiated following ingestion of gluten in genetically predisposed individuals [ 189 , 190 ]. Research has suggested that dysbiosis plays a role in triggering coeliac disease with a dysregulated immune response and failure to maintain intestinal barrier integrity, leading to mucosal inflammation [ 191 ]. However, like IBD, it remains unclear as to whether the dysbiotic state characteristic of coeliac disease is a cause or consequence of a dysregulated immune response.…”

“…As coeliac disease generally presents in childhood and young adulthood, most studies looking at a link between coeliac disease and the microbiome have focused on children [ 191 ]. Rod-shaped bacteria, including Clostridia, Provotella, and Actinomyces, are more frequently found in the small bowel of children with active coeliac compared with healthy controls [ 192 ].…”

Probiotics: Versatile Bioactive Components in Promoting Human Health

“…Celiac disease (celiac disease) is the only autoimmune disease in which both the trigger, the epigenetic factor (gluten), but also the specific HLA antigen (human leukocyte antigen) are known. Unfortunately, celiac disease is underdiagnosed, and people with or without GI manifestations, symptomatic and asymptomatic subjects can be found [ 52 ]. Dysbiosis can promote celiac disease, and recent studies have established a link between dietary gluten (wheat, oats, barley, rye) and changes in the intestinal microbiome.…”

Distinctive Microbial Signatures and Gut-Brain Crosstalk in Pediatric Patients with Coeliac Disease and Type 1 Diabetes Mellitus

“…An imbalance of the gut microbiota composition, called microbial dysbiosis, is characterized by decreased microbial diversity, gain or loss of specific community members or changes in their relative abundance [ 49 ]. A wide array of studies have identified significant differences in the microbial diversity and taxonomic composition of gut microbial communities between healthy controls and patients with CD [ 44 , 50 , 51 , 52 ] or T1DM [ 53 , 54 , 55 ]. However, the specific microbial taxonomic differences vary widely depending on the study design, and a definitive disease-associated community structure has not been identified.…”