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Publication
Bacteria: Potential Make-or-Break Determinants of Celiac Disease
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Advisor(s)
Abstract(s)
Celiac 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.
Description
Funding: This research was supported by a 2022 Beyond Celiac Established Investigator Award
(BeyondCeliac.org) and by Fundação para a Ciência e Tecnologia under the grants UIDB/05704/2020
for the research unit, UI/BD/151038/2021 for Ana Roque, and CEECINST/00051/2018
(https://doi.org/10.54499/CEECINST/00051/2018/CP1566/CT0004) for Sónia Gonçalves Pereira.
Keywords
Bacteria Microbiota Host–microbe interactions Disease mechanisms Celiac disease
Citation
Roque, A.; Pereira, S.G. Bacteria: Potential Make-or-Break Determinants of Celiac Disease. Int. J. Mol. Sci. 2024, 25, 2090. https:// doi.org/10.3390/ijms25042090
Publisher
MDPI