Short-term effects of Poly(I:C) on gut permeability

Moyano-Porcile, Valentina; Olavarría-Ramírez, Loreto; González-Arancibia, Camila; Bravo, Javier A.; Julio–Pieper, Marcela

doi:10.1016/j.phrs.2015.06.016

Cited by 16 publications

(11 citation statements)

References 38 publications

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“…Dysregulation of these processes, or excessive TLR activation, can result in chronic inflammatory and over-exuberant repair responses. Recent evidence suggests that the TLR3 synthetic agonist, Poly(I:C) not only decreases epithelial resistance in the small intestine but also promoted thinning of the mucosal layer (Moyano-Porcile et al, 2015 ).…”

Section: Candidate Pathways To Barrier Dysfunctionmentioning

confidence: 99%

Breaking down the barriers: the gut microbiome, intestinal permeability and stress-related psychiatric disorders

Kelly

Kennedy

Cryan

et al. 2015

Front. Cell. Neurosci.

836

624

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The emerging links between our gut microbiome and the central nervous system (CNS) are regarded as a paradigm shift in neuroscience with possible implications for not only understanding the pathophysiology of stress-related psychiatric disorders, but also their treatment. Thus the gut microbiome and its influence on host barrier function is positioned to be a critical node within the brain-gut axis. Mounting preclinical evidence broadly suggests that the gut microbiota can modulate brain development, function and behavior by immune, endocrine and neural pathways of the brain-gut-microbiota axis. Detailed mechanistic insights explaining these specific interactions are currently underdeveloped. However, the concept that a “leaky gut” may facilitate communication between the microbiota and these key signaling pathways has gained traction. Deficits in intestinal permeability may underpin the chronic low-grade inflammation observed in disorders such as depression and the gut microbiome plays a critical role in regulating intestinal permeability. In this review we will discuss the possible role played by the gut microbiota in maintaining intestinal barrier function and the CNS consequences when it becomes disrupted. We will draw on both clinical and preclinical evidence to support this concept as well as the key features of the gut microbiota which are necessary for normal intestinal barrier function.

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Section: Candidate Pathways To Barrier Dysfunctionmentioning

confidence: 99%

Breaking down the barriers: the gut microbiome, intestinal permeability and stress-related psychiatric disorders

Kelly

Kennedy

Cryan

et al. 2015

Front. Cell. Neurosci.

836

624

View full text Add to dashboard Cite

show abstract

“…Paracellular permeability and TJ were found to be significantly ameliorated when mice were pretreated with poly I:C, as demonstrated by decreased FITC-D permeability, ameliorated ultrastructural changes, and enhanced expression of TJ proteins at the both mRNA and protein levels. The direct effect of poly I:C on intestinal barrier function has been investigated in vitro by Moyano-Porcile et al[ 28 ], and indicated that acute exposure of rat ileum and colon tissues to poly I:C reduced colon permeability to macromolecules, while increasing ileum permeability to micromolecules. Intraperitoneal injection of poly I:C has been reported to cause severe mucosal injury of the small intestine, along with the increased levels of IL-15[ 16 ].…”

Section: Discussionmentioning

confidence: 99%

Effect of toll-like receptor 3 agonist poly I:C on intestinal mucosa and epithelial barrier function in mouse models of acute colitis

Zhao

Yue

Han

et al. 2017

WJG

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AIMTo investigate potential effects of poly I:C on mucosal injury and epithelial barrier disruption in dextran sulfate sodium (DSS)-induced acute colitis.METHODSThirty C57BL/6 mice were given either regular drinking water (control group) or 2% (w/v) DSS drinking water (model and poly I:C groups) ad libitum for 7 d. Poly I:C was administrated subcutaneously (20 μg/mouse) 2 h prior to DSS induction in mice of the poly I:C group. Severity of colitis was evaluated by disease activity index, body weight, colon length, histology and myeloperoxidase (MPO) activity, as well as the production of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin 17 (IL-17) and interferon-γ (IFN-γ). Intestinal permeability was analyzed by the fluorescein isothiocyanate labeled-dextran (FITC-D) method. Ultrastructural features of the colon tissue were observed under electron microscopy. Expressions of tight junction (TJ) proteins, including zo-1, occludin and claudin-1, were measured by immunohistochemistry/immunofluorescence, Western blot and real-time quantitative polymerase chain reaction (RT-qPCR).RESULTSDSS caused significant damage to the colon tissue in the model group. Administration of poly I:C dramatically protected against DSS-induced colitis, as demonstrated by less body weight loss, lower disease activity index score, longer colon length, colonic MPO activity, and improved macroscopic and histological scores. It also ameliorated DSS-induced ultrastructural changes of the colon epithelium, as observed under scanning electron microscopy, as well as FITC-D permeability. The mRNA and protein expressions of TJ protein, zo-1, occludin and claudin-1 were also found to be significantly enhanced in the poly I:C group, as determined by immunohistochemistry/immunofluorescence, Western blot and RT-qPCR. By contrast, poly I:C pretreatment markedly reversed the DSS-induced up-regulated expressions of the inflammatory cytokines TNF-α, IL-17 and IFN-γ.CONCLUSIONOur study suggested that poly I:C may protect against DSS-induced colitis through maintaining integrity of the epithelial barrier and regulating innate immune responses, which may shed light on the therapeutic potential of poly I:C in human colitis.

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“…However, tissue viability is a major concern and therefore incubation times no longer than 3 h are recommended (Clarke, 2009). The use of everted gut sacs to measure the transit of fluorescent probes has the advantage of not demanding specialized equipment, but larger amounts of tissue are required (3–4 cm 2 ) (Moyano-Porcile et al, 2015; Eyzaguirre-Velasquez et al, 2017). In the Ussing chamber, ion transport across the intestinal wall can be measured in very small segments of tissue (1 cm 2 ) but a more expensive setup is necessary.…”

Section: Methods For Testing Gut Permeability and Other Markers Of Bamentioning

confidence: 99%

Investigating Gut Permeability in Animal Models of Disease

et al. 2019

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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.

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Short-term effects of Poly(I:C) on gut permeability

Cited by 16 publications

References 38 publications

Breaking down the barriers: the gut microbiome, intestinal permeability and stress-related psychiatric disorders

Breaking down the barriers: the gut microbiome, intestinal permeability and stress-related psychiatric disorders

Effect of toll-like receptor 3 agonist poly I:C on intestinal mucosa and epithelial barrier function in mouse models of acute colitis

Investigating Gut Permeability in Animal Models of Disease

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