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- Bacteria: Potential Make-or-Break Determinants of Celiac DiseasePublication . Roque, Ana; Pereira, Sónia GonçalvesCeliac disease is an autoimmune disease triggered by dietary gluten in genetically susceptible individuals that primarily affects the small intestinal mucosa. The sole treatment is a gluten-free diet that places a social and economic burden on patients and fails, in some, to lead to symptomatic or mucosal healing. Thus, an alternative treatment has long been sought after. Clinical studies on celiac disease have shown an association between the presence of certain microbes and disease outcomes. However, the mechanisms that underlie the effects of microbes in celiac disease remain unclear. Recent studies have employed disease models that have provided insights into disease mechanisms possibly mediated by bacteria in celiac disease. Here, we have reviewed the bacteria and related mechanisms identified so far that might protect from or incite the development of celiac disease. Evidence indicates bacteria play a role in celiac disease and it is worth continuing to explore this, particularly since few studies, to the best of our knowledge, have focused on establishing a mechanistic link between bacteria and celiac disease. Uncovering host–microbe interactions and their influence on host responses to gluten may enable the discovery of pathogenic targets and development of new therapeutic or preventive approaches.
- Dietary patterns drive loss of fiber-foraging species in the celiac disease patients gut microbiota compared to first-degree relativesPublication . Roque, Ana; Zanker, Joyce; Brígido, Sara; Tomaz, Maria Beatriz; Gonçalves, André; Barbeiro, Sandra; Benítez-Páez, Alfonso; Pereira, Sónia GonçalvesBackground Celiac disease is an autoimmune disorder triggered by dietary gluten in genetically predisposed indi‑viduals that primarily afects the small intestine. Studies have reported diferentially abundant bacterial taxa in the gut microbiota of celiac patients compared with non-celiac controls. However, fndings across studies have inconsisten‑cies and no microbial signature of celiac disease has been defned so far. Results Here, we showed, by comparing celiac patients with their non-celiac 1st-degree relatives, that bacterial com‑munities of related individuals have similar species occurrence and abundance compared with non-relatives, regard‑less the disease status. We also found in celiac patients a loss of bacterial species associated with fber degradation,and host metabolic and immune modulation, as ruminiclostridia, ruminococci, Prevotella, and Akkermansia muciniphila species. We demonstrated that the diferential abundance of bacterial species correlates to diferent dietary pat‑terns observed between the two groups. For instance, Ruminiclostridium siraeum, Ruminococcus bicirculans, and Bacteroides plebeious, recognized as fber-degraders, appear more abundant in non-celiac 1st-degree relatives, which havea vegetable consumption pattern higher than celiac patients. Pattern of servings per day also suggests a possible link between these species’ abundance and daily calorie intake. Conclusions Overall, we evidenced that a kinship approach could be valuable in unveiling potential celiac disease microbial traits, as well as the signifcance of dietary factors in shaping microbial profles and their infuence on dis‑ease development and progression. Our results pave the way for designing and adopting novel dietary strategies based on gluten-free fber-enriched ingredients to improve disease management and patients’ quality of life.
- Influence of commensal bacteria on the proteolytic and antigenic profiles of INFOGEST-like digested wheat gliadinPublication . Pereira-Costa, Flávio; Domingues, Vanessa S.; Roque, Ana; Almeida, Zaida L.; Cruz, Pedro F.; Cordeiro, Rachel; Trindade, Daniela; Moura, Carla; Melo, Joana B.; Pereira, Sónia G.; Vaz, Daniela C.Introduction: Celiac disease (CeD) is a chronic autoimmune enteropathy developed by genetically predisposed individuals when exposed to gluten. Gluten gliadins, along with gut microbiota, may influence CeD onset and progression through mechanisms that remain unclear. Methods: Gliadin-degrading bacterial isolates obtained from CeD patients, and their 1st-degree relatives’ stool and blood were identified (Bacillus tropicus, Enterococcus faecalis, Micrococcus sp., Cronobacter sakazakii, Pseudomonas aeruginosa, and Serratia marcescens) and used in an INFOGEST-like protocol to simulate gliadin digestion after 4 h (digested gliadin, d-gliadin). The d-gliadin digesta were analyzed by fast protein liquid chromatography (FPLC), dynamic light scattering (DLS), Fourier transform infrared spectroscopy (FTIR), scanning electron microscopy (SEM), fluorescence spectroscopy, and polyclonal and monoclonal (R5 and G12) enzyme-linked immunosorbent assays (ELISA). Results and discussion: In the absence of the bacterial isolates, gliadin is poorly digested and self-assembles within 1 day into intermediate and large protein oligomers/aggregates, enriched in β-sheet structure (FTIR amide I band between 1,600 and 1,700 cm−1) and able to bind thioflavin T and Congo red. Conversely, in the presence of the bacterial isolates, gliadin is further digested, leading to an increase in protein fragments. After 4 h, the P. aeruginosa, C. sakazakii, and B. tropicus d-gliadin digesta presented a mixture of d-gliadin peptides and aggregates that showed higher antigenicity (associated with the exposure of the 5-amino acid QQPFP and 6-amino acid QPQLPY epitopes, present in the 25-mer and 33-mer, respectively) than control digestions (without bacteria), while E. faecalis led to lower antigenicity. In turn, within 24 h of incubation, all bacterial isolates led to the formation of undigested material with lower antigenicity, either due to fewer 33-mers and 25-mers in solution, or to fragment aggregation into amorphous material, not exposing antigenic sequences. Hence, intestinal flora may enhance or diminish the antigenicity of gliadin, thereby modulating the immunogenic response to gliadin/gluten.