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      A nanoparticle platform for combined mucosal healing and immunomodulation in inflammatory bowel disease treatment

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          Abstract

          Current treatments for inflammatory bowel disease (IBD) treatment consist of anti-inflammatory products. In this study, we sought to induce the physiological secretion of glucagon-like peptide 2, a peptide with intestinal growth-promoting activity, via nanoparticles while simultaneously providing with immunomodulation by tailoring the nanoparticle surface. To this end, we developed hybrid lipid hyaluronate-KPV conjugated nanoparticles loaded with teduglutide for combination therapy in IBD. The nanocarriers induced (or did not induce) immunosuppression depending on the presence (or absence) of a hyaluronan-KPV functionalization. This strategy holds promise as a nanoparticle platform for combined mucosal healing and immunomodulation in IBD treatment.

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          • •

            We have demonstrated that lipid nanocapsules per se increased GLP-2 secretion in vitro and in vivo in a murine acute colitis model.

          • •

            We tested the mucosal healing and anti-inflammatory properties of the formulation, demonstrating no immunomodulatory effect of the nanocarriers.

          • •

            Hyaluronan-KPV functionalized teduglutide-loaded nanocarriers combined anti-inflammatory and mucosal healing properties upon intermittent administration.

          • •

            The pharmacological effect exerted by our nanocarriers induced sufficient stimulus as per providing with mucosal healing upon intermittent administration of our formulation.

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          Most cited references42

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          PKSolver: An add-in program for pharmacokinetic and pharmacodynamic data analysis in Microsoft Excel.

          Yong Zhang, Meirong Huo, Jianping Zhou … (2010)
          This study presents PKSolver, a freely available menu-driven add-in program for Microsoft Excel written in Visual Basic for Applications (VBA), for solving basic problems in pharmacokinetic (PK) and pharmacodynamic (PD) data analysis. The program provides a range of modules for PK and PD analysis including noncompartmental analysis (NCA), compartmental analysis (CA), and pharmacodynamic modeling. Two special built-in modules, multiple absorption sites (MAS) and enterohepatic circulation (EHC), were developed for fitting the double-peak concentration-time profile based on the classical one-compartment model. In addition, twenty frequently used pharmacokinetic functions were encoded as a macro and can be directly accessed in an Excel spreadsheet. To evaluate the program, a detailed comparison of modeling PK data using PKSolver and professional PK/PD software package WinNonlin and Scientist was performed. The results showed that the parameters estimated with PKSolver were satisfactory. In conclusion, the PKSolver simplified the PK and PD data analysis process and its output could be generated in Microsoft Word in the form of an integrated report. The program provides pharmacokinetic researchers with a fast and easy-to-use tool for routine and basic PK and PD data analysis with a more user-friendly interface. Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
          Article 0 comments Cited 496 times – based on 0 reviews     Review now
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            Changes in gut microbiota control inflammation in obese mice through a mechanism involving GLP-2-driven improvement of gut permeability

            P D Cani, S Possemiers, T Van de Wiele … (2009)
            Background and aims: Obese and diabetic mice display enhanced intestinal permeability and metabolic endotoxaemia that participate in the occurrence of metabolic disorders. Our recent data support the idea that a selective increase of Bifidobacterium spp. reduces the impact of high-fat diet-induced metabolic endotoxaemia and inflammatory disorders. Here, we hypothesised that prebiotic modulation of gut microbiota lowers intestinal permeability, by a mechanism involving glucagon-like peptide-2 (GLP-2) thereby improving inflammation and metabolic disorders during obesity and diabetes. Methods: Study 1: ob/ob mice (Ob-CT) were treated with either prebiotic (Ob-Pre) or non-prebiotic carbohydrates as control (Ob-Cell). Study 2: Ob-CT and Ob-Pre mice were treated with GLP-2 antagonist or saline. Study 3: Ob-CT mice were treated with a GLP-2 agonist or saline. We assessed changes in the gut microbiota, intestinal permeability, gut peptides, intestinal epithelial tight-junction proteins ZO-1 and occludin (qPCR and immunohistochemistry), hepatic and systemic inflammation. Results: Prebiotic-treated mice exhibited a lower plasma lipopolysaccharide (LPS) and cytokines, and a decreased hepatic expression of inflammatory and oxidative stress markers. This decreased inflammatory tone was associated with a lower intestinal permeability and improved tight-junction integrity compared to controls. Prebiotic increased the endogenous intestinotrophic proglucagon-derived peptide (GLP-2) production whereas the GLP-2 antagonist abolished most of the prebiotic effects. Finally, pharmacological GLP-2 treatment decreased gut permeability, systemic and hepatic inflammatory phenotype associated with obesity to a similar extent as that observed following prebiotic-induced changes in gut microbiota. Conclusion: We found that a selective gut microbiota change controls and increases endogenous GLP-2 production, and consequently improves gut barrier functions by a GLP-2-dependent mechanism, contributing to the improvement of gut barrier functions during obesity and diabetes.
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              Chemically induced mouse models of acute and chronic intestinal inflammation

              Stefan Wirtz, Vanessa Popp, Markus Kindermann … (2017)
              This protocol update describes how to generate mouse models of inflammatory bowel diseases and methods for analyzing disease progression.
              Article 0 comments Cited 394 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Ana Beloqui
                Journal
                Journal ID (nlm-ta): Bioact Mater
                Journal ID (iso-abbrev): Bioact Mater
                Title: Bioactive Materials
                Publisher: KeAi Publishing
                ISSN (Electronic): 2452-199X
                Publication date PMC-release: 11 October 2023
                Publication date Collection: February 2024
                Publication date (Electronic): 11 October 2023
                Volume: 32
                Pages: 206-221
                Affiliations
                [a ]UCLouvain, Université catholique de Louvain, Louvain Drug Research Institute, Advanced Drug Delivery and Biomaterials, 1200 Brussels, Belgium
                [b ]UCLouvain, Université catholique de Louvain, Louvain Drug Research Institute, Bioanalysis and Pharmacology of Bioactive Lipids, 1200 Brussels, Belgium
                [c ]UCLouvain, Université catholique de Louvain, Institute of Experimental and Clinical Research, Laboratory of Hepato-Gastroenterology, 1200 Brussels, Belgium
                [d ]Cliniques universitaires Saint-Luc, Department of Hepato-Gastroenterology, Brussels, Belgium
                [e ]EM-platform, VIB Bio Imaging Core, KU Leuven, Campus Gasthuisberg, Herestraat 49, 3000 Leuven, Belgium
                [f ]UCLouvain, Université catholique de Louvain, Louvain Drug Research Institute, Metabolism and Nutrition Group, 1200 Brussels, Belgium
                [g ]UCLouvain, Institute of Experimental and Clinical Research, 1200 Brussels, Belgium
                [h ]WEL Research Institute, Avenue Pasteur, 6, 1300 Wavre, Belgium
                Author notes
                [∗ ]Corresponding author. Université catholique de Louvain, Louvain Drug Research Institute, Advanced Drug Delivery and Biomaterials, 1200 Brussels, Belgium. ana.beloqui@ 123456uclouvain.be
                [1]

                Equal contribution.

                Article
                Publisher Item ID: S2452-199X(23)00297-9
                DOI: 10.1016/j.bioactmat.2023.09.014
                PMC ID: 10582360
                PubMed ID: 37859689
                SO-VID: 98a6f6b8-99b5-4ddd-ab88-cb27e7cef9d9
                Copyright © © 2023 The Authors
                License:

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 13 July 2023
                Date revision received : 19 September 2023
                Date accepted : 22 September 2023
                Categories
                Subject: Article

                Keywords: nanocarrier,glp-2,teduglutide,kpv,inflammatory bowel disease
                Data availability:
                Keywords: nanocarrier, glp-2, teduglutide, kpv, inflammatory bowel disease

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