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Targeting immunoproteasome and glutamine supplementation prevent intestinal hyperpermeability. | LitMetric

Targeting immunoproteasome and glutamine supplementation prevent intestinal hyperpermeability.

Biochim Biophys Acta Gen Subj

Normandie Univ, INSERM unit 1073, Nutrition, Inflammation and Gut-brain axis, Rouen, France; Rouen University, Institute for Research and Innovation in Biomedicine, Rouen, France; Department of Nutrition, Rouen University Hospital, Rouen, France. Electronic address:

Published: January 2017

AI Article Synopsis

Article Abstract

Background: Intestinal hyperpermeability has been reported in several intestinal and non-intestinal disorders. We aimed to investigate the role of the ubiquitin proteasome system in gut barrier regulation in two mice models: the water avoidance stress model (WAS) and a post-inflammatory model (post-TNBS).

Methods: Both models were applied in C57BL/6 male mice (n=7-8/group); Proteasome was targeted by injection of a selective proteasome inhibitor or by using knock-out mice for β2i proteasome subunit. Finally, glutamine supplementation was evaluated.

Results: In both models (WAS at day 10, post-TNBS at day 28), we observed an increase in proteasome trypsin-like activity and in inducible β2/constitutive β2 subunit protein expression ratio, associated with an increase in intestinal permeability. Moreover, intestinal hyperpermeability was blunted by intraperitoneal injection of selective proteasome inhibitor in WAS and post-TNBS mice. Of note, knock-out mice for the β2i subunit exhibited a significant decrease in intestinal permeability and fecal pellet output during WAS. Glutamine supplementation also improved colonic permeability in both models.

Conclusions: In conclusion, the proteasome system is altered in the colonic mucosa of WAS and post-TNBS mice with increased trypsin-like activity. Associated intestinal hyperpermeability was blunted by immunoproteasome inhibition.

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Source
http://dx.doi.org/10.1016/j.bbagen.2016.08.010DOI Listing

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