Coeliac disease involves immune-mediated damage to the small intestine after gluten exposure in genetically susceptible individuals, with increased intestinal permeability recognized as a central pathophysiological feature. The literature summarized describes mechanisms that may disrupt barrier integrity, including the role of zonulin, proinflammatory cytokines, microbial alterations, and gliadin peptide–driven immune responses. Evidence for permeability changes is discussed in the context of disease activity and remission, though the strength and consistency of data across studies are not detailed here. Therapies aiming to restore barrier function are reviewed, encompassing dietary modifications and supplements, as well as experimental and investigational pharmacologic agents such as larazotide acetate and IMU-856. The article also emphasizes the need for reliable biomarkers to quantify intestinal permeability in coeliac disease and calls for continued research into barrier-normalising strategies as a means to sustain remission. Where data are incomplete or uncertain in the reviewed sources, this ambiguity is acknowledged. No specific clinical outcomes or comparative effectiveness data are provided in the summary presented.
Coeliac disease is characterised by immune-mediated damage to the small intestine in response to dietary gluten in genetically predisposed individuals. Increased intestinal permeability is a central component to its pathophysiology. This review explores the evidence for increased permeability in coeliac disease and the underlying mechanisms, including the roles of zonulin, inflammatory cytokines, microbial alterations and immune responses to gliadin peptides. We also review comprehensively the therapies targeting barrier integrity and normalising intestinal permeability, including particular diets and supplements, and experimental and improved medications including larazotide acetate and IMU-856. Finally, we highlight the need for reliable biomarkers for evaluating increased permeability in coeliac disease and advocate for further research on therapies which normalise barrier function, particularly as a strategy to maintain remission.