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Abstract
A growing number of investigations report the association between gut permeability and intestinal or extra-intestinal disorders under the basis that translocation of gut luminal contents could affect tissue function, either directly or indirectly. Still, in many cases it is unknown whether disruption of the gut barrier is a causative agent or a consequence of these conditions. Adequate experimental models are therefore required to further understand the pathophysiology of health disorders associated to gut barrier disruption and to develop and test pharmacological treatments. Here, we review the current animal models that display enhanced intestinal permeability, and discuss (1) their suitability to address mechanistic questions, such as the association between gut barrier alterations and disease and (2) their validity to test potential treatments for pathologies that are characterized by enhanced intestinal permeability.
Highlights
Many clinical disorders are characterized or accompanied by GI alterations, including symptoms such as discomfort or pain, bloating and altered motility which can negatively impact a patient’s quality of life
Many functional, cellular and biochemical features of the intestinal barrier are conserved among species; for example, a high degree of similarity is observed between tight junction proteins across vertebrates (Robinson et al, 2015; Brugman, 2016)
Empiric evidence obtained from animal models, including correlation studies and mechanistic designs allow us to propose particular aspects of barrier function as potential pathways to disease
Summary
Many clinical disorders are characterized or accompanied by GI alterations, including symptoms such as discomfort or pain, bloating and altered motility which can negatively impact a patient’s quality of life. Being constantly exposed to microbes and potentially damaging or immunogenic substances (i.e., bacterial, dietary and xenobiotic components and their metabolites) it requires a selective and efficient barrier function Increased permeability via the transcellular but especially the paracellular pathway can allow for excessive translocation of microbial and diet-derived molecules, potentially contributing to inflammatory conditions (Galipeau and Verdu, 2016) Another gut epithelial cell type are enteroendocrine cells, capable of releasing endocrine mediators. Immersed in the intestinal epithelium are immune cells which upon contact with luminal material are able to coordinate adequate responses either to prevent microbial invasion (Li et al, 2012) or to dampen down exaggerated immune reactions (Turner, 2009) These mucosal immune cells exert modulatory functions over the intestinal barrier; for example, T helper cell-derived cytokines can help modify the flux of molecules across tight junctions or cation pores (Turner, 2009). Many functional, cellular and biochemical features of the intestinal barrier are conserved among species; for example, a high degree of similarity is observed between tight junction proteins across vertebrates (Robinson et al, 2015; Brugman, 2016)
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