Microbiome in Celiac Disease: Changes in microbial profile along the gastrointestinal tract revealed by 16S rRNA high throughput gene sequencing

Background: Numerous immune-mediated diseases have been linked to shifts in the gut microbiome's composition, including celiac disease (CeD). CeD is an autoimmune disease characterised by gluten intolerance developed in genetically susceptible individuals under environmental factors. The microbiome can modulate the immune response by the action of short-chain fatty acids (SCFA) and degrade immunogenic peptides of gluten through endoprolyl peptidase enzymes. Studies profiling the microbiome in CeD describe an alteration in the patient's intestinal microbiome leading to a dysregulated immune response that contributes to its pathogenesis. However, there is no consensus containing all the microbial changes associated with this pathology and the possible use of microbiome for diagnosis, evaluation of disease progression, or as a target for treatment. 

Materials: We perform a scoping review of the studies profiling the microbiome in CeD patients by 16S rRNA high-throughput sequencing (2010-2020). Also, we performed an analysis combining the multiple datasets available to get a consensus. Moreover, we predict microbial communities' functional and metabolic capacities. 

Results. We analysed the diversity, taxonomic composition, and functional potential of the microbiome in the duodenum, saliva, faeces and pharynx of 168 patients with CeD and 192 healthy controls. A reduction in microbial diversity was observed in CeD, and differences were detected in the abundance and prevalence of specific taxa, according to each part of the gastrointestinal tract (GIT). An increase in gram-negative commensals with pathogenic potential and decreased beneficial commensals SCFA producers were observed (Figure). No differences were found in the abundance of endoprolyl peptidases. There was a decrease in genes involved in the production of SCFAs. Additionally, increased metabolic pathways indicative of inflammation were found.

Conclusion: We could detect specific changes in CeD patients' microbiome and modifications in SCFA production and inflammation genes across the GIT. More differentially abundant taxa were found in the lower GIT than in the upper one, suggesting that CeD has a more significant impact on these tissues' microbial communities. Further studies are needed to evaluate these changes and the possible use of microbial biomarkers found for diagnosis, following the diseases' progression, as evaluating gut microbiota's potential as an adjuvant treatment in CeD.