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Dissertations / Theses on the topic 'Permeabilità intestinale'

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Published: 11 March 2023

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1

Ponce, de Leon Rodriguez Maria del Carmen. "Développement d’un modèle in vitro d’inflammation intestinale par l’utilisation de lignées cellulaires humaines en co-culture pour l’étude des interactionsavec les micro-constituants alimentaires." Thesis, Montpellier, 2019. http://www.theses.fr/2019MONTG009/document.

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L’épithélium intestinal, siège de l’absorption des (micro)-nutriments est aussi le premier système de défense de l’organisme. Un déséquilibre dans l’homéostasie peut être à l’origine d’une réaction inflammatoire associée à des défauts de la barrière intestinale et de la fonction immunitaire, ainsi qu’une malabsorption des nutriments, comme rencontré dans les MICI (Maladies Inflammatoires Chroniques de l’Intestin), dans les stratégies de fortification en micronutriments et les pathologies non transmissibles (obésité). Il est donc important de trouver des moyens d’action, via l’alimentation par exemple, pour prévenir ou au minima réduire, les conséquences nutritionnelles et pathologiques de l’inflammation intestinale, et de comprendre les mécanismes impliqués. Parmi les modèles d’études de l’intestin, les modèles in vitro de culture cellulaire sont de plus en plus utilisés et permettent d'évaluer les mécanismes moléculaires d'une manière simple et reproductible et de réduire l'expérimentation animale.Dans ce contexte et dans le but d’étudier l’interaction de composés bioactifs de l’alimentation avec l’intestin en état d’inflammation, le premier objectif de ce travail de thèse a été la mise au point d’un modèle in vitro d’intestin enflammé associant en co-culture deux lignées intestinales humaines : les Caco-2 TC7 (entérocytes) et HT29-MTX (cellules caliciformes) et une lignée immunitaire de macrophages (THP1). Plusieurs marqueurs d’inflammation ont été évalués et nous avons pu montrer que le modèle de tri-culture répondait à un stimulus inflammatoire (LPS/IFNγ), par une augmentation de la production de cytokines pro-inflammatoires (TNF-α, IL6 et IL8) et d’enzymes (INOS et COX2) ainsi que l’expression de leurs gènes. Par ailleurs, une augmentation de la perméabilité épithéliale via une altération des jonctions serrées (TJs) a également pu être mise en évidence ainsi qu’une surproduction de mucus, lesquels sont des caractéristiques reconnus d’inflammation.Le deuxième objectif était d’étudier l’interaction de la β-cryptoxanthine (BCX), caroténoïde des agrumes, lipophile et anti-oxydant, avec le modèle enflammé. Nous avons utilisé pour solubiliser la BCX deux types de micelles (artificielles et physiologiques) et étudié les marqueurs d’inflammation. Bien qu’il semble d’après les résultats préliminaires que les micelles de BCX montrent une tendance à diminuer la production de certaines cytokines (IL6 et IL8), le rôle des constituants des micelles (Tween 40 ou sels biliaires/phospholipides) dans ce phénomène observé et dans la perméabilité épithéliale reste à clarifier par la suite
The intestinal epithelium, main place of the absorption of (micro)-nutrients is also the first body's defense system. An imbalance in homeostasis can lead to an inflammatory reaction associated with defects in the intestinal barrier and immune function as well as malabsorption of nutrients, as seen in IBD (Inflammatory Bowel Diseases), in micronutrient fortification strategies and noncommunicable diseases (obesity). It is therefore important to find ways of action, for example through diet, to prevent or at least reduce the nutritional and pathological consequences of intestinal inflammation, and to understand the mechanisms involved. Among intestinal models, in vitro cell culture models are increasingly used and allow to evaluate the molecular mechanisms in a simple and reproducible way and to reduce animal experimentation.In this context and in order to study the interaction of dietary bioactive compounds with the intestine in state of inflammation, the first objective of this work was the development of an in vitro model of inflamed intestine combining in co-culture two human intestinal cell lines: Caco-2 TC7 (enterocytes) and HT29-MTX (goblet cells) and an immune cell line of macrophages (THP1). Several inflammation markers were evaluated and we were able to show that the tri-culture model responded to an inflammatory stimulus (LPS / IFNγ), by increasing the production of pro-inflammatory cytokines (TNF-α, IL6 and IL8) and enzymes (INOS and COX2) as well as the expression of their genes. In addition, an increase of epithelial permeability via tight junctions (TJs) alteration has also been demonstrated, as well as overproduction of mucus, which are recognized inflammation characteristics.The second objective was to study the interaction of β-cryptoxanthin (BCX), a lipophilic and antioxidant carotenoid of citrus, with the inflamed model. To solubilize BCX, we used two types of micelles (artificial and physiological) and studied markers of inflammation. Although it appears from the preliminary results that BCX micelles show a tendency to decrease the production of some cytokines (IL6 and IL8), the role of micelle constituents (Tween 40 or bile salts / phospholipids) in the phenomenon observed and in the epithelial permeability remains to be therefore clarified
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2

Weaver, Laurence Trevelyan. "The intestinal permeability of infants." Thesis, University of Cambridge, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289788.

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3

Smethurst, Paul R. "Small intestinal permeability in man." Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315531.

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4

Lundin, Pål. "Intestinal permeability a parameter of mucosal dysfunction /." Lund : Dept. of Animal Physiology, Lund University, 1997. http://books.google.com/books?id=wuNqAAAAMAAJ.

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5

Lang, Mia E. "Intestinal permeability in the irradiated ferret." Thesis, University of Ottawa (Canada), 1991. http://hdl.handle.net/10393/7772.

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Ferrets received whole-body irradiation (5 Gy, gamma). At different times post-irradiation (PIRR, 2, 24, and 48 hours), measurements of fluid and electrolyte fluxes, and of the blood-to-lumen clearance of $\sp{51}$Cr-EDTA, were compared between in situ perfused loops of jejunum and ileum. Intestinal permeation of $\sp{51}$Cr-EDTA was increased (4x control) in both the jejunum and ileum at 2 hours PIRR. At 24 hours PIRR, $\sp{51}$Cr-EDTA permeation was the same as control. At 48 hours PIRR, jejunal permeation of $\sp{51}$Cr-EDTA was not statistically different from control animals, whereas in the ileum, $\sp{51}$Cr-EDTA permeation was increased 10x control. Absorption of luminal fluid was abolished 2 hours PIRR in the ileum. Sodium and chloride fluxes were unaffected by radiation exposure, but at 48 hours PIRR there was a significant secretion of potassium in the ileum. Diarrhea rarely occurred after the first hour post-irradiation. Serotonin, acting via 5-HT$\sb3$ receptors, was investigated as a possible mediator of radiation-induced alterations in intestinal permeability. Pretreatment with the 5-HT$\sb3$ antagonist and anti-emetic BRL 43694 significantly reduced the severity of radiation-induced vomiting. It offered some therapeutic benefit to radiation-induced diarrhea. However BRL 43694 pretreatment had no effect on intestinal permeability. (Abstract shortened by UMI.)
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6

Anderson, Alexander Douglas Gray. "Measurement of intestinal permeability in surgical patients." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/24575.

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Aim: The aim of this study was to investigate the use of a triple sugar test of intestinal permeability as a surrogate marker of gut barrier function in surgical patients. Methods: Original laboratory work included the development of a technique for the quantification of urinary sucralose using high performance liquid chromatography (HPLC) with refractive index detection. Other techniques used included HPLC analysis of urinary lactulose and rhamnose, quantification of urinary 51Cr-EDTA by gamma counting, and a lactulose-hydrogen breath test. The triple sugar test involved ingestion of a test drink containing sucralose (5g), lactulose (5g) and rhamnose (1g). Urine was collected for 24 hours in 2 aliquots (first 5 and last 19 hours) and sugar concentrations determined by HPLC. A 51Cr-EDTA test was administered separately as an independent measure of “whole-gut” permeability. Healthy volunteers (n=21) and ileostomists (n=18) were studied in order to investigate the sites of absorption of sugar probes. A number of patient groups were then studied; these included subjects with Crohn’s disease (n=16),acute colitis (n=18), IBS (n=11), acute pancreatitis (n=9) and patients undergoing chemotherapy (n=7). Results: Assays for urinary sugars were both accurate and precise (coefficient of variation approximately 5%). Studies in ileostomists and controls indicated that 24-hr sucralose excretion represented “whole-gut” permeability, whereas the 5-hr lactulose/rhamnose excretion ratio represented small intestinal permeability. Small intestinal permeability was increased in subjects with Crohn’s disease (p=0.007) and acute pancreatitis (p=0.004), versus controls. “Whole gut” permeability was significantly increased in patients with Crohn’s (p=0.001) and pancreatitis (p<0.001), and significantly reduced in patients undergoing chemotherapy (p=0.012). The proportion of sucralose excreted in the last 19 hours of collection was significantly increased in patients with Crohn’s (p=0.026), acute colitis (0.023) and acute pancreatitis (p=0.049), implying an increase in colonic permeability.
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7

Salameh, Emmeline. "Développement d'un modèle murin de dénutrition avec entéropathie et évaluation de molécules d'intérêt permettant de contribuer au rétablissement de la fonction de barrière intestinale." Thesis, Normandie, 2019. http://www.theses.fr/2019NORMR064.

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Contexte : La malnutrition aiguë sévère (MAS) est un problème majeur de santé publique dans lemonde et affecte 17 millions d’enfants âgés de moins de 5 ans. La MAS induit une perte de poidsrapide, souvent associée à une dysfonction entérique environnementale (DEE). La DEE se caractérisepar une augmentation de l’inflammation, de la perméabilité intestinale, une diminution de la taille des villosités et de l’absorption des nutriments. La DEE peut ainsi limiter l’efficacité des protocolesde stabilisation et de re-nutrition chez l’enfant dénutri.L’objectif de cette thèse a été de développer un modèle de dénutrition avec entéropathie pour évaluer des laits thérapeutiques enrichis en nutriments ciblant la fonction de barrière intestinale.Résultats : Lors de la phase de développement du modèle, plusieurs approches ont été testées comme la restriction calorique, le régime hypoprotéiné, l’utilisation de lipopolysaccharides et de l’indométacine. Seule la combinaison d’un gavage quotidien d’indométacine pendant une semaine chez des souris dénutries par un régime pauvre en protéines a permis de développer un retard de croissance associé à une entéropathie. Suite à la validation de ce modèle, nous avons évalué la supplémentation du lait thérapeutique F-75 avec de la glutamine, de la leucine, de la gomme arabique et des levures séléniées. La glutamine et la leucine améliorent la fonction de barrière intestinale. Dans nos conditions expérimentales, l’enrichissement du lait thérapeutique avec la glutamine et la leucine combinés a eu des effets limités sur la fonction de barrière. La gomme arabique et les levures séléniées ont des propriétés prébiotiques et probiotiques et exercent des effets bénéfiques sur la barrière intestinale. L’enrichissement du lait thérapeutique avec l’association de ces deux composés permet d’inhiber l’inflammation intestinale et d’augmenter l’abondance de bactéries bénéfiques comme Faecalibacterium prausnitzii.Conclusion : Les travaux réalisés au cours de cette thèse ont permis de développer un nouveau modèle de dénutrition avec entéropathie. Le lait thérapeutique enrichi en gomme arabique et levures séléniées exerce des effets bénéfiques sur la fonction de barrière intestinale dans notre modèle
Background : Severe acute malnutrition (SAM) is a global health issue affecting 17 million children under the age of 5. SAM induces rapid weight loss and is often associated with environmental enteric dysfunction (EED). EED is characterized by intestinal hyperpermeability and inflammation, villus blunting and nutrient malabsorption. EED might, therefore, limit stabilization and re-nutrition protocol efficacy. Objectives : This thesis aimed to develop an undernutrition model with enteropathy to evaluate the effect of a therapeutic milk enriched with nutrients on gut barrier function. Results : During preclinical model development, several approaches were tested: calorie restriction, low-protein diet, use of lipopolysaccharides and indomethacin. Only daily indomethacin gavage during one week in protein-energy undernourished mice induced growth faltering associated with enteropathy. After preclinical model validation, we evaluated the effect of therapeutic milk supplemented with glutamine, leucine, gum arabic and/or selenium-enriched yeast on gut barrier function. Glutamine and leucine induce beneficial effects on gut barrier function. In ourexperimental conditions, therapeutic milk enriched with a combination of glutamine and leucine had a limited impact on this parameter. Gum arabic and selenium-enriched yeasts have prebiotic and probiotic properties on gut barrier function. Therapeutic milk supplemented with gum arabic and selenium-enriched yeast inhibited intestinal inflammation and enhanced specific bacteria abundance such as Faecalibacterium prausnitzii.Conclusion : The studies conducted during this thesis permitted to develop a new model of undernutrition with enteropathy. Therapeutic milk enriched with arabic gum and selenium-enriched yeast triggered beneficial effects on gut barrier function in our preclinical model
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8

Yao, Shengtao. "The effect of denervation on intestinal permeability and function following small intestinal transplantation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq22692.pdf.

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9

Wang, Chuan. "Pathologically and experimentally induced intestinal barrier changes evaluated by permeability measurements." Lund : Dept. of Animal Physiology, Lund University, 1995. http://books.google.com/books?id=ddlqAAAAMAAJ.

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10

Bahlouli, Wafa. "Régulation de la perméabilité intestinale au cours du syndrome de l'intestin irritable : role du système ubiquitine-protéasome et impact de l'obésité." Thesis, Normandie, 2019. http://www.theses.fr/2019NORMR047.

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Le syndrome de l’intestin irritable (SII) est un trouble fonctionnel d’origine multifactorielle, impliquant des facteurs environnementaux tels que le stress, l’alimentation et met en jeu un dysfonctionnement de l’axe intestin-cerveau, une micro-inflammation, une dysbiose et une hyperperméabilité intestinale. Le rôle du protéasome dans la régulation de la barrière intestinale au cours du SII a été étudié. De plus, ces troubles fonctionnels intestinaux (TFI) ont également été décrits comme exacerbés chez des patients souffrant d’obésité, dont la physiopathologie est complexe. Néanmoins, les mécanismes impliqués dans cette association restent mal compris et ont donc été recherchés. Dans ce travail, des modèles murins « SII-like » comme le modèle de stress « water avoidance stress » ou WAS et le modèle post-inflammatoire « post-TNBS » ont été utilisés afin d’étudier l’impact d’une inhibition du protéasome sur la régulation de la perméabilité intestinale. L’inhibition pharmacologique du protéasome par le PR-957 ou l’utilisation de souris invalidées pour une sous unité β2i du protéasome limite l’hyperperméabilité intestinale. Une supplémentation orale en glutamine permet également de diminuer la perméabilité intestinale. Une étude protéomique au niveau colique des souris WAS et une étude de l’ubiquitome colique de patients souffrant de SII à profil diarrhéique confirment l’implication du protéasome dans la physiopathologie du SII. Nous avons ensuite cherché à comprendre le lien entre l’obésité et le SII en combinant des modèles d’obésité (génétique et induite par une alimentation riche en graisses ou HFD) et le modèle WAS. Seules les souris HFD présentent une exacerbation de l’hyperperméabilité intestinale et une corticostéronémie plasmatique élevée en réponse au modèle WAS. Des études complémentaires suggèrent que ces résultats sont indépendants de la leptine, de la glycémie et du microbiote intestinal. Nos travaux proposent donc de nouvelles pistes de prise en charge des patients souffrant de SII, par intervention nutritionnelle via la glutamine ou en utilisant le protéasome comme cible thérapeutique. Nous suggérons également un rôle de l’alimentation (riche en graisse) dans le développement des TFI au cours de l’obésité
Irritable bowel syndrome (IBS) is a multifactorial functional disorder, involving environmental factors (stress and diet for instance), gut-brain-axis dysfunction, micro-inflammation, dysbiosis and an alteration of intestinal permeability. The role of the proteasome in the regulation of the intestinal barrier during IBS has been studied. In addition, these intestinal functional disorders have also been described in patients with obesity. Nevertheless, the mechanisms underlying an association of intestinal functional disorders in the obesity context, remain poorly understood and have therefore been investigated in this thesis. In this study, "IBS-like" mouse models such as water avoidance stress (WAS) and the post-inflammatory (post-TNBS) models, were used to study the impact of proteasome inhibition on the regulation of intestinal permeability. We found that the pharmacological inhibition of the proteasome (with PR-957) or the use of knock-out mice for a subunit of the proteasome (β2i -/-) limit intestinal hyperpermeability occured in IBS-Like models. Moreover, we found that oral supplementation with glutamine also reduces intestinal hyperpermeability, wich, thus, can be considered as a putative nutritional treatment for IBS. A colonic proteomic study of WAS mice and a study of colonic ubiquitoma in IBS patients with diarrheal profiles confirmed the involvement of proteasome in the pathophysiology of IBS. Therefore, the link between obesity and IBS was examined by combining models of obesity (ob/ob genetic and high-fat diet [HFD] models) with WAS model. Only HFD mice displayed enhanced intestinal hyperpermeability and higher plasma corticosterone levels in response to WAS. Further studies suggest that these results, themselve, are independent of leptin, glycaemia and gut microbiota. This study paves new ways of treating patients suffering from IBS, by nutritional intervention via glutamine or by using the proteasome as a therapeutic target. We also suggest a role of diet (high fat) in the development of intestinal functional disorders during obesity
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11

Benoit, Bérengère. "Effet des acides gras alimentaires à chaîne longue sur la barrière épithéliale colique." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10239.

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Les cellules à mucus intestinales sécrètent des mucines, principalement MUC2, qui forment un gel protecteur. Malgré la place importante des acides gras à chaîne longue (AGCL) dans l'alimentation et leurs liens avec des pathologies où les cellules à mucus sont altérées il n'existe pas d'étude sur leurs impacts sur ces cellules. Mes travaux ont consisté à mettre en lumière ces interactions et à étudier leurs conséquences. In vitro, nous montrons que les AGCL saturés augmentent l'expression de MUC2 et son relarguage alors que les AGCL insaturés les inhibent et que l'acide palmitique favorise la différenciation cellulaire. In vivo, chez des ratons gavés avec de l'huile de palme, la production de MUC2 est augmentée et la perméabilité paracellulaire colique diminuée. Les huiles de colza ou de tournesol ne modifient pas la production de MUC2 et la perméabilité est identique aux contrôles malgré l'augmentation de l'expression de l'occludine. Dans un modèle de syndrome de l'intestin irritable, nous montrons que le gavage avec l'huile de palme, malgré la diminution de l'occludine, restaure la perméabilité et augmente le nombre de cellules à mucus. L'huile de colza et l'huile de tournesol ne corrigent pas le défaut de perméabilité. Parallèlement, deux études chez la souris ont mis en évidence l'impact de certains régimes sur le nombre des cellules à mucus. Ce travail a permis d'identifier les AGCL comme des nutriments capables de moduler les cellules à mucus, de faire émerger une nouvelle piste thérapeutique pour restaurer les populations de cellules à mucus et la perméabilité et d'ouvrir la réflexion sur les impacts de l'augmentation des populations de cellules à mucus chez l'individu sain
Intestinal goblet cells secrete mucins, mainly MUC2, which form a protective mucus gel. Despite the important place of long chain fatty acids (LCFA) in the diet and their links with pathologies where goblet cells are altered, there is no study dealing with their impact on goblet cells. The aim of my work was to highlight these interactions and to study their consequences. In vitro, we show that saturated LCFA increase MUC2 expression and release whereas unsaturated LCFA inhibit these process and that palmitic acid promotes cellular differentiation. In vivo, rat pups receiving oral administration of palm oil show a decrease of colonic paracellular permeability and an increase of MUC2 production. On the opposite, rapeseed and sunflower oils do not change MUC2 production and, intestinal permeability is the same as controls despite the increase of occludin expression. In an animal model of irritable bowel syndrome, palm oil effects are found again. When subjected rat pups to a maternal deprivation stress a few days after birth, they develop an intestinal hyperpermeability and a goblet cell depletion. We show that oral administration of palm oil concomitantly to the stress is able to, despite a decrease of occludin expression, restore the permeability at the level of non-stressed animals and to increase goblet cell number. Rapeseed oil and sunflower oil are not able to correct the increase of intestinal permeability. In parallel, studies in mice show that some types of diets can be associated with an increase of the number of proximal and distal goblet cells. To conclude, this work (i) helped to identify LCFA as nutrients able to modulate intestinal goblet cell number and physiology, (ii) put forward a new therapeutic track, via palmitic acid use, to restore goblet cell populations and intestinal permeability in pathologies associated with these kind of alterations and finally (iii) offered new tracks of reasoning about physiological and pathophysiological impacts of the increase of intestinal goblet cell number in a healthy subject
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12

Stenberg, Patric. "Computational models for the prediction of intestinal membrane permeability." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-4934-4/.

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13

Alhamoruni, Abdissalam Ag Ali. "In vitro studies of huam intestinal permeability and modulation." Thesis, University of Nottingham, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.537654.

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14

Genser, Laurent. "Etude de la perméabilité intestinale au cours de l'obésité humaine." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066645.

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Chez les rongeurs rendus obèses par un régime hyper-lipidique, un changement du microbiote est associé à une altération de la perméabilité intestinale, augmentant le passage d’antigènes alimentaires ou bactériens et contribuant à une inflammation chronique de bas grade et une insulinorésistance. Cependant chez l’homme, les modifications de perméabilité intestinale, son impact sur les altérations métaboliques, inflammatoires systémiques et tissulaires sont peu documentées. L’objectif de ce travail est de caractériser la perméabilité intestinale (i.e. jéjunum) et les mécanismes impliqués dans sa régulation dans l’obésité humaine sévère en conditions de jeûne (basal) et après un apport aigu de lipides selon des approches complémentaires in vivo (biomarqueurs), ex vivo (chambre de Ussing, étude des protéines de jonctions serrées en immunofluorescence) et in vitro (lignée cellulaire Caco-2/TC7). A l’état basal nous avons observé une diminution de la localisation de l’occludine et de la tricelluline dans les jonctions serrées au niveau du jéjunum et des taux circulants en zonuline et LPS binding protéine plus élevés chez les obèses. La perméabilité Jéjunale basale mesurée ex vivo en chambre de Ussing était comparable entre obèses et non obèses avec cependant des liens entre ces mesures et les paramètres de l’inflammation systémique chez les patients obèses (CRP et Haptoglobine). Une charge unique en lipides alimentaires, entrainait une augmentation rapide et significative de la perméabilité aux macromolécules (FITC-Dextran 4 kDa) in vitro et ex vivo, démontrant ainsi l’effet direct des lipides postprandiaux sur la barrière épithéliale. La perméabilité aux macromolécules après exposition aux lipides était plus élevée chez les patients obèses à fortiori diabétiques de type 2 et était associée à l’inflammation systémique (CRP) et intestinale (calprotectine fécale). Ainsi, nos résultats mettent en évidence un défaut de la barrière intestinale dans l'obésité caractérisée par une hyperperméabilité jéjunale démasquée par les lipides alimentaires et associée à l’inflammation et aux troubles métaboliques
Intestinal barrier damage is associated with low-grade inflammation and metabolic impairment in rodent models of obesity. Whether intestinal permeability is altered in human metabolic disorders remains poorly investigated. Using a large cohort of well-characterized obese subjects and a human enterocyte model, we examined intestinal permeability in the basal state and after a challenge by a lipid load. We showed a reduction of occludin and tricellulin at jejunal tight junctions and increased serum levels of zonulin and LPS-Binding Protein in obese subjects. Jejunal permeability, directly measured in Ussing chambers in the fasting condition, was not significantly increased compared to non-obese subjects. Nevertheless, within the obese cohort, high permeability was associated with systemic inflammation (CRP and haptoglobin). A single lipid load increased permeability both in Caco-2/TC7 cells and ex vivo in human jejunum, demonstrating dietary lipids’ direct effects on the epithelial barrier. Permeability after the lipid load was significantly higher in the jejunum of obese subjects and associated with systemic and intestinal inflammation (CRP and fecal calprotectin) and type 2 diabetes. Thus, our results highlight an intestinal barrier defect in obesity, with a jejunal permeability increased by a lipid challenge and linked to inflammatory and metabolic impairments
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15

ANCEL, DAVID BIGARD MARC-ANDRE. "COMPARAISON DE LA PERMEABILITE INTESTINALE ENTRE CIRRHOSE ETHYLIQUE ET CIRRHOSE VIRALE." [S.l.] : [s.n.], 2001. http://www.scd.uhp-nancy.fr/docnum/SCDMED_T_2001_ANCEL_DAVID.pdf.

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16

Yadav, Vipul. "Intestinal stability and permeability of anti-TNF α monoclonal antibodies." Thesis, University College London (University of London), 2017. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.724210.

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17

Willemsen, Linette Eustachia Maria. "Intestinal barrier function: regulation of epithelial permeability and mucin expression." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2004. http://dare.uva.nl/document/74526.

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18

Hoorelbeke, Anne. "Evaluation de la scintigraphie de permeabilite alveolaire et intestinale dans la sclerodermie." Lille 2, 1991. http://www.theses.fr/1991LIL2M303.

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DIAMANTE, BARBARA. "PROPRIETA' FUNZIONALI DELLA BARRIERA INTESTINALE DI INSETTO E MODULAZIONE DELLA PERMEABILITA' PARACELLULARE." Doctoral thesis, Università degli Studi di Milano, 2012. http://hdl.handle.net/2434/168386.

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Control of insect pests is still mainly performed using broad spectrum chemical pesticides even though the limits of this strategy are presently well known: the reduction in pest population is associated with an unfavourable alteration of food quality and safety, with a strong impact on nontarget species and with the rise of a widespread resistance in target insects. The most recent approach to the Integrated Pest Management is based on the detection of new genes encoding for polypeptides with potential insecticide activity, with a particular attention to biopesticides derived from insect antagonists and plants (Whetstone e Hammock, 2007). However, efficient delivery methods are essential in deploying bioinsecticides. For an effective oral delivery, it will be crucial to develop strategies to facilitate their passage through the midgut barriers, i.e. the peritrophic membrane (PM) and the midgut epithelium (ME). This can be achieved by altering the sieving properties of the PM and by increasing the rate of absorption by the ME. In the framework of a coordinated effort towards the development of new delivery strategies my laboratory, in collaboration with other research groups, discovered that the recombinant Chitinase A (ChiA) of Autographa californica multicapsid nucleopolyhedrovirus (AcMNPV) determined in vitro structural alterations on lepidopteran larvae PM and a strong increase of its permeability to molecules (Rao et al., 2004). Moreover, when this enzyme is delivered either with artificial diet or with transgenic plants to lepidopteran larvae, a significant negative effect on insect biological performance and survival was observed. I demonstrated that PMs isolated from fifth instar Heliothis virescens larvae fed on transgenic tobacco plants expressing ChiA starting from the first day of the fourth instar show an increased flux of methylene blue. The PMs were mounted in Ussing chambers and incubated in the presence of methylene blue, a good tracer of PM permeability, in the endoperitrophic compartment. The flux of methylene blue through the PMs isolated from larvae reared on ChiA-expressing tobacco plants was significantly higher than that of controls (PM isolated from larvae reared on control tobacco plants). To demonstrate that the increased permeability was due to the hydrolytic activity of AcMNPV ChiA on the PM chitin mesh, this enzyme was extracted and purified from ChiA-expressing tobacco plants and its activity tested on the permeability of PMs of H. virescens larvae isolated in Ussing chambers. PM incubation with ChiA (40 μM) in the endoperitrophyc compartment caused a significant increase of TMOF (Trypsin Modulating Oostatic Factor) flux compared to control. Thus, the use of this enzyme, and of any other similar enhancer, can be of great interest in the development of effective delivery strategies. Once crossed the PM, the macromolecules have to pass the ME. They can reach the haemocoel either through the cellular pathway, crossing the two polarized plasma membranes of the epithelial cells, or through the paracellular pathway, along the aqueous channels formed by the junctional complexes. The latter, a preeminent pathway for the delivery of small peptides (Fiandra et al. 2009), is the main objective of my study. In my lab a number of functional properties of the smooth septate junction (SJ) of the lepidopteran larval midgut has been recently elucidated in vitro, demonstrating that its permeability can be modulated by cAMP and/or a fine regulation of cytosolic Ca2+ concentration (Fiandra et al., 2006). During my PhD, I have studied one of the signaling pathway(s) that may lead to the intracellular release of Ca2+ responsible for the increase of the junction permeability. I took advantage of a medium-chain fatty acid (C10) known to modulate the mammalian tight junction by activation of a Ca2+ ions-mediated intracellular signaling pathway (Cano-Cebrian et al., 2005). I demonstrated that the addition of C10 (20 mM) to the luminal side of Bombyx mori larval midguts isolated in conventional Ussing chambers, caused a decrease of the paracellular (shunt) electrical resistance (Rsh) (i.e. an increase of the junction ion conductance) and an increase of the paracellular fluxes of proctolin and fluorescein, two molecules that cross the midgut epithelium only through the paracellular route. Afterward, I evaluated if the effect of C10 on the shunt electrical resistance in lepidopteran larvae was due to the activation of a Ca2+ ions-mediated intracellular signaling pathway like in the mammalian tight junction, i.e. if C10 induced a raise of the intracellular calcium concentration. B. mori midgut cells, obtained by enzymatic disaggregation of the tissue, were pre-loaded with the cell permeant Ca2+-sensitive fluorescent dye Fluo-3AM, incubated in the absence (control) or in the presence of C10 (2 mM) and observed by fluorescence microscopy. Control cells did not show an appreciable fluorescence intensity during the entire experimental period. On the contrary, midgut cells incubated with C10 for 5 min showed a strong fluorescence signal, no more observable after 10 min of incubation. These data demonstrate that C10 causes a transient increase of the free cytosolic calcium concentration and therefore that its effect on the shunt resistance can be due, like in mammals, to the activation of a Ca2+ ions-mediated intracellular signaling pathway. Then, I analyzed which is the signalling pathway activated by C10 that leads to the raise of the intracellular calcium concentration in lepidopteran midgut cells. I examined whether specific inhibitors of major proteins involved in signal cascade activated by C10 in mammalian cells were able to abolish the decrease of the paracellular resistance induced by C10 on B. mori larval midgut. The inhibitors used are: U-73122, inhibitor of phospholipase C (PLC), W-7 inhibitor of calcium-calmodulin binding, ML-7 and PEPTIDE-18, which inhibit the kinase responsible for phosphorylation of the myosin light chain (MLCK). Then I calculated the value of the paracellular resistance in the midgut of B. mori larvae mounted in Ussing chamber in the presence of C10 or in the presence C10 and inhibitors. The results obtained indicate that all the inhibitors tested are able to abolish the effect caused by the C10 on Rsh. Summarizing the data, I demonstrated that C10 triggers an IP3- dependent signalling cascade by activation of phopholipase C. As a result, Ca2+ is released from the intracellular stores and a calmodulin-dependent kinase is activated. This event leads to the phosphorylation of the myosin light chain by myosin light chain kinase. Myosin light chain phosphorylation presumably causes a modification of the cytoskeleton organization connected to the SJ and thereby an increase of the paracellular permeability to ions and small organic molecules. Even though the study of the permeability through the peritrophic membrane and the paracellular pathway represents the main part of my PhD project, I have also collaborated to the characterization of the early events involved in Junonia coenia densovirus (JcDNV) infection of the lepidopteran pest Spodoptera frugiperda. A few years ago my laboratory has begun a collaboration with Dr. Mylene Ogliastro (“Laborotoire de Biologie Integrative et Virologie” INRA-UMII - Institute National de la Researche Agronomique-Université de Montpellier II-, France) with the aim to clarify some aspects of JcDNV pathogenicity. Densoviruses (DNVs) are parvoviruses highly pathogenic for arthropods, mostly insects, at larval stages, including agronomical pests and insects vector-borne diseases (Bergoin, 2008). DNVs have a limited host-range and are not pathogenic to vertebrates, characteristics that make them particularly interesting as potential pest control agents alternative to chemical pesticides. During the second year of my PhD I spent a period in Montpellier, in Dr. Ogliastro’s lab, where I collaborated to the elucidation of the mechanism used by JcDNV to enter midgut columnar cells. Midguts of S. frugiperda larvae were isolated, cut longitudinally and interposed as a sheet between the two half chambers of the Ussing perfusion apparatus. Midguts were preincubated for 30 min in the absence (control) or in the presence of different drugs: dynasore, (400 μM) that inhibits clathrin-coated vesicle formation blocking the GTPase dynamine, the sterol-sequestering drug methyl cyclodextrine (60 μM) that inhibits lipid raft-dependent endocytosis and the fungal toxin wortmannin (10 mM), a PI3K inhibitor. Virus was then added to the luminal compartment and the incubation lasted 10 min. To verify if these drugs inhibit JcDNV internalization we performed immunofluorescence assays. Midguts incubated with the drugs did not present virus particles inside the cells or, however, a lesser amount compared to control sample, a clear indication that clathrin mediated endocytosis, lipid-raft dependent endocytosis and PI3K-dependent pathways are involved in JcDNV internalization. These data indicate that JcDNV uptake into midgut columnar cells of S. frugiperda larvae is mediated by different endocytic mechanisms. This finding is not surprising, since a number of viruses have been shown to utilize more than one pathway for internalization.
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20

Zamora, Samuel A. "Crohn's disease, investigation of intestinal permeability across families of affected children." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq24714.pdf.

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21

Tannergren, Christer. "Intestinal Permeability and Presystemic Extraction of Fexofenadine and R/S-verapamil." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3971.

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22

Ruttenberg, David. "Intestinal permeability to polyethylene glycol 400 in patients with Crohn's disease." Master's thesis, University of Cape Town, 1993. http://hdl.handle.net/11427/25587.

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An altered small intestinal permeability has been proposed as an important aetiological factor in the pathogenesis of inflammatory bowel disease. The relevant literature was reviewed. Intestinal permeability to Polyethylene glycol 400 in patients with Crohn' s disease, their relatives and healthy controls was examined and the data compared with studies of small bowel permeability to other similar sized probes. A new technique of analysis of urinary Polythylene Glycol 400 by High Performance Liquid Chromatography was described and compared with a previously established HPLC method. No evidence of an altered bowel permeability could be found using Polyethylene glycol 400, but the possibility that this may have been related to probe size and characteristics can not be excluded .
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23

Rubelt, Miriam. "Enhancement of the intestinal epithelial permeability of peripherally acting opioid analgesics by chitosan." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2013. http://dx.doi.org/10.18452/16864.

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Die schmerzstillende Wirkung von Opiaten wird über Opioidrezeptoren im zentralen und peripheren Nervensystem vermittelt. Die Schmerzlinderung kann jedoch mit sehr starken Nebenwirkungen einhergehen, die das Patientenwohlbefinden beeinträchtigen. Dies legt die Bedeutung von neuen Opioidanalgetika nahe, die ihre schmerzstillende Wirkung ausschließlich über Opioidrezeptoren im PNS entfalten, ohne unerwünschte zentrale Nebenwirkungen zu induzieren. Die orale Gabe von Medikamenten minimiert Unannehmlichkeiten für den Patienten, jedoch müssen die Substanzen die intestinale Barriere passieren können, um in die Blutzirkulation eintreten zu können. Die intestinale Permeabilität von zwei peripher wirksamen Opiaten (AS006 und Loperamid) wurde in Ussing-Kammer Experimenten untersucht. Um die Darmepithelpermeabilität für beide Opiate zu erhöhen, wurde der Absorptionsverstärker Chitosan verwendet. Chitosan bewirkte nach 30 Minuten bei HT29/B6 und Caco-2 Zelllinien eine Abnahme des epithelialen Widerstands in vitro. Die Permeabilität für AS006 war bei beiden Zelllinien erhöht, für Loperamid nur bei HT29/B6, jedoch nicht bei Caco-2 Zellmonolayern. Verhaltensexperimente zur Messung des antinozizeptiven Effektes von oral appliziertem Loperamid auf Entzündungsschmerz wurden an Ratten durchgeführt. Die orale Gabe von Loperamid induzierte eine Dosis-abhängige antinozizeptive Wirkung in der entzündeten Hinterpfote. Bei oraler Gabe von Loperamid in Kombination mit Chitosan wurde keine signifikante Verstärkung des maximalen antinozizeptiven Effekts von Loperamid beobachtet. Zusammenfassend ist Chitosan ein geeigneter Absorptionsverstärker für intestinale Permeabilitätsstudien von peripher wirksamen Opioidanalgetika in vitro. Die in vitro Ergebnisse haben gezeigt, dass der Effekt von Chitosan auf Loperamid möglicherweise schwächer ist als auf AS006. Dementsprechend fiel die Wirkung des Absorptionsverstärkers auf Loperamid-induzierte Analgesie im Verhaltensversuch eher gering aus.
Analgesic effects of opioids are mediated by opioid receptors that are widely distributed in the central and peripheral nervous systems (CNS and PNS, respectively). Although opioids are the most powerful analgesics, severe side effects restrict their use and affect patient convalescence. This suggests an advantage of new analgesic opioids which selectively bind to opioid receptors in the PNS. After oral administration however, peripherally restricted opioids first have to cross the intestinal epithelial barrier before absorption into the circulation and distribution to opioid receptors in peripheral tissues. Here, the transport across intestinal epithelia of two opioid ligands (AS006 and loperamide) that selectively activate peripheral opioid receptors without entering the CNS were investigated. To increase the intestinal passage of these drugs, the absorption enhancer chitosan was used. Chitosan significantly decreased the transepithelial resistance of HT29/B6 and Caco-2 cell monolayers after 30 min in vitro. The permeability values for AS006 increased from < 0.3 × 10-6 cm/s up to 10 × 10-6 cm/s in the presence of chitosan. In contrast, HT29/B6 monolayers showed moderate loperamide permeability in the presence of chitosan, and chitosan had no effect on the permeability of loperamide using Caco-2 monolayers. Oral administration of loperamide induced a dose-depended elevation of paw pressure thresholds in inflamed paws that lasted for 60 min. Oral administration of loperamide combined with chitosan slightly but nonsignificantly enhanced the antinociceptive effect of loperamide. In conclusion, chitosan is a suitable absorption enhancer for in vitro intestinal permeability studies. Future in vivo experiments might investigate different formulations and application schedules, and further address the effects of chitosan on the antinociceptive efficacy of hydrophilic opioids.
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24

COLLET, REGIS. "Anomalies de la permeabilite pulmonaire dans la maladie de crohn : relations avec la permeabilite intestinale et le lavage broncho-alveolaire." Lille 2, 1989. http://www.theses.fr/1989LIL2M307.

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25

Høst, Jan. "In silico predicition of intestinal transport /." Cph. : The Danish University of Pharmaceutical Sciences, 2006. http://www.dfuni.dk/index.php/Jan_Hoest/3066/0/.

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26

Bours, Martijn Jan Leo. "Role of extracellular ATP in immunity and intestinal defence effects on intestinal permeability and enterocyte-driven inflammatory response /." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Universiteit Maastricht [host], 2007. http://arno.unimaas.nl/show.cgi?fid=9328.

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27

Bajka, Balazs Hendrik. "The characterization of an in vitro model of small intestinal permeability dysfunction /." Title page and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09SB/09sbb165.pdf.

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28

CASULA, EMANUELA. "Probiotic Lactobacillus strains attenuate oxysterols-induced alteration of human intestinal membrane permeability." Doctoral thesis, Università degli Studi di Cagliari, 2021. http://hdl.handle.net/11584/312980.

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The intestinal membrane is an important structure which carries out central functions such as nutrient absorption and excretion and secretion of several products and acts as a barrier to protect the human body from potentially harmful compounds arriving from diet; foods are sources of both potentially dangerous and potentially protective molecules. When a noxious stimulus occurs, it can alter membrane balance and functionality, mostly by altering the tight junctions, increasing its permeability, or causing a shift on microbiota composition and thus sustaining inflammation. Inflammation and oxidative stress have been linked to the loss of intestinal integrity, a crucial event in the initiation and progression of pathological intestinal disorders such as inflammatory bowel diseases (IBD) and cancer. Oxysterols are cholesterol oxidative products, which have been reported to act negatively on intestinal membrane, causing an increase in its permeability and a local inflammation. On the other hand, several studies reported probiotics and short chain fatty acids (SCFAs), produced by the microbiota, as able to exert anti-inflammatory properties and to improve gut barrier permeability. In this context, the aim of this research project was to evaluate the capacity of two probiotic strains of Lactobacillus (Lactobacillus plantarum 299v® (DMS 9843) and Lactobacillus casei DG® (CNCMI1572), used as bacterial extract or live culture, to protect intestinal epithelium against the alteration of permeability induced by oxysterols and to investigate the mechanism of action in relation to tight junctions modulation and cellular signaling. A preliminary study was also conducted to investigate any modifications induced by oxysterols or probiotics on the metabolic activity of the gut resident bacteria. To achieve this objective, monolayers of differentiated Caco-2 cells have been used as in vitro model of intestinal barrier, and a batch culture system, to mimic the colonic environment. The alteration of cell monolayers permeability, treated with oxysterols alone or together with the bacterial extract or live culture was evaluated through the measurement of transepithelial electrical resistance (TEER), in relation to the modulation of tight junctions, occludin, zonulin and JAM-A, linked to MAPKs, p38 and ERK1/2 activation. Batch culture system have been inoculated with a human faecal sample in a basal media added with oxysterols and/or the bacterial extract or the live culture of the two different strains of the lactobacillus in order to evaluate, possible changes in microbiota SCFAs production. Our results provide, for the first time, evidence of the ability of Lactobacillus spp. probiotics to protect intestinal cells against the pro-inflammatory effect of oxysterols, in vitro. We observed a protective effect turned toward one key inflammatory mechanism such as the alteration of the intestinal permeability, caused by the oxysterols-induced TJs disruption, due, at least in part, to the modulation of MAPK/p38 pathway. The similar efficacy exerted by the bacterial extracts and the pure cultures, suggest a promising effect of both probiotic strains tested as bacterial extracts in the treatment of intestinal inflammation, avoiding the stimulation of the immune system, which is a side effect of the use of the commercialised pure cultures. Regarding batch cultures, we did not detect any significant interaction among oxysterols, probiotics and intestinal microbiota metabolic activity in the experimental condition used; this part of the research project is a preliminary study which we aim to enrich with further investigations. Taken together our data strengthen the link between diet and intestinal inflammation and encourages us to continue studying probiotics as a useful tool in the prevention and management of the most common intestinal pathologies linked to the inflammatory process.
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Adenis, Antoine. "Etude de la permeabilite intestinale et pulmonaire au cours de la maladie de crohn." Lille 2, 1989. http://www.theses.fr/1989LIL2M097.

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30

Foster, Russell. "Modulation of intestinal permeability with special reference to the absorption of bioactive peptides." Thesis, King's College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281711.

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31

Gertz, Michael. "Prediction of intestinal availability in human from in vitro clearence and permeability data." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.503642.

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32

TRISAL, PREETI. "IMPACT OF NONIONIZABLE GLYCOL SOLUBILIZERS EXHIBITING DIFFERENT SURFACE ACTIVITIES ON INTESTINAL MEMBRANE PERMEABILITY." University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1116005486.

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33

Bidu, Célia. "Résistance des souris transgéniques fat-1 à l'obésité : prévention de l'endotoxémie métabolique et modulation du microbiote intestinal par les acides gras polyinsaturés en n-3." Thesis, Dijon, 2015. http://www.theses.fr/2015DIJOS058/document.

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L’obésité est associée à un état inflammatoire chronique de bas grade ainsi qu’à descomplications métaboliques secondaires telles que l’insulino-résistance, l’intolérance au glucose etla stéatose hépatique. La composition bactérienne intestinale semble tenir une place importantedans l’apparition de ces complications. Il a en effet été montré qu’une altération du microbiote parun régime obésogène était associée à une endotoxémie métabolique caractérisée par uneaugmentation des concentrations circulantes de lipopolysaccharides bactériens. Les AGPI enn-3 possèdent des propriétés anti-obésogènes et anti-inflammatoires qui pourraient passer par unemodulation du microbiote intestinal et une prévention de l’endotoxémie métabolique. Nous avonsmontré que des souris transgéniques fat-1, présentant des teneurs tissulaires en AGPI enn-3 élevées, soumises durant 18 semaines à un régime obésogène, étaient résistantes à l’obésité etaux troubles métaboliques associés. Ces animaux présentent un maintien de la fonction barrièreintestinale et une prévention de l’endotoxémie métabolique. De plus, une analyse du microbiotecaecal révèle une augmentation du phylum Akkermansia. Enfin, nous avons montré qu’un transfertde matériel fécal de souris fat-1 à des souris sauvages maintenues sous régime obésogène protègeces dernières du développement d’une obésité et des comorbidités associées. Ainsi, uneaugmentation de la teneur en Akkermansia au niveau intestinal par les AGPI en n-3, peutreprésenter une stratégie intéressante de prévention de l’obésité, ainsi que de l’insulino-résistance,l’intolérance au glucose et la stéatose hépatique qui lui sont associées
Obesity is associated with chronic low-grade inflammatory state and secondary metabolicdisorders, such as insulin-resistance, glucose intolerance and hepatic steatosis. Gut microbiotaseems to play an important role in these obesity features. Moreover, microbiota dysbiosis has beenshown to be associated with increased systemic lipopolysaccharides levels, called metabolicendotoxemia. N-3 PUFAs are anti-obesity and anti-inflammatory molecules able to modulate gutmicrobiota and prevent metabolic endotoxemia. We showed that fat-1 transgenic mice,endogenously synthetizing n-3 PUFAs, resist to obesity development and comorbidities whensubmitted to diet-induced obesity for 18 weeks. These mice exhibit a maintained intestinal barrierfunction and a prevention of metabolic endotoxemia. Moreover, cecal microbiota analysis revealedan increase of Akkermansia phylum. Microbiota transplantation of fat-1 mice to wild type micewas shown to exert protective effects against diet-induced obesity and associated disorders. Thus,increasing gut microbiota Akkermansia population by appropriate n-3 PUFAs may represent apromising strategy to prevent obesity, insulin-resistance, glucose intolerance and hepatic steatosis
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Esser, Dirk Michael [Verfasser]. "Veränderungen der intestinalen Permeabilität bei operierten Morbus Crohn Patienten / Dirk Michael Esser." Köln : Deutsche Zentralbibliothek für Medizin, 2010. http://d-nb.info/1001963970/34.

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35

Chamignon, Célia. "Identification de souches bactériennes à potentiel probiotique dans la diminution des hyperperméabilités intestinales et détermination de leur(s) mécanisme(s) d’action." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASA011.

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Le tractus gastro-intestinal représente la plus grande interface entre le corps humain et son environnement. Il s'agit d'un système multicouches composé de mucus et de cellules épithéliales établissant et régulant des barrières, tout en se connectant directement au système immunitaire. Cette interface permet les flux d'eau et de nutriments et empêche l'entrée des toxines et des pathogènes. C'est donc la première ligne de défense. La régulation de la perméabilité se produit essentiellement par la voie para-cellulaire, elle-même soutenue par le complexe épithélial de protéines de jonction. Le microbiote intestinal joue un rôle clé dans la régulation des systèmes immunitaire et métabolique ainsi que dans la protection contre les agents pathogènes. Les interactions continues entre la barrière intestinale et le microbiote sont essentielles pour maintenir l'intégrité intestinale et donc l'homéostasie globale dans des conditions saines. De nos jours, la plupart des syndromes ou maladies chroniques, comme le syndrome de l’intestin irritable (SII) mais aussi les troubles métaboliques ou comportementaux, sont associés à une augmentation de la perméabilité intestinale, aussi appelée « syndrome de l'intestin qui fuit ». En effet, l'hyperperméabilité a pour conséquence une augmentation du flux d’eau et de nutriments, à travers l’épithélium intestinal, mais surtout des pathogènes et des toxines, favorisant une réponse immunitaire et une inflammation. De nombreuses études ont aussi associé des changements de la composition du microbiote intestinal, dysbiose, aux maladies chroniques. Les effets bénéfiques des souches probiotiques sont de plus en plus démontrés à la fois dans des études in vitro jusqu’à des essais cliniques, et montrent qu’ils peuvent être utilisés non seulement dans des approches préventives mais également thérapeutiques. Nous avons voulu comprendre les interactions entre les composants épithéliaux intestinaux et les bactéries probiotiques dans le contexte physiopathologique des troubles chroniques intestinaux. Pour cela, nous avons mis en place un criblage de plus de cinquante souches bactériennes, provenant de genres différents, sur des modèles de perméabilité in vitro basés sur la résistance électrique trans-épithéliale (TEER) et utilisant deux types de lignées cellulaires intestinales humaines, Caco-2 et T84. Ces modèles nous ont permis de sélectionner six souches de Lactobacillus que nous avons caractérisées sur leurs propriétés probiotiques (capacité d’adhésion, stabilité de la forme biofilm, production de neurotransmetteurs et activité enzymatique). Nous avons ensuite évalué les bénéfices de certaines d’entre elles dans des modèles in vivo d’inflammation chronique de bas grade et de séparation maternelle néonatale, utilisant des souris C57BL/6J. Nous avons finalement déterminé l’implication des souches bactériennes sur la modulation de la perméabilité intestinale via l’étude du complexe de protéines de jonction cellulaire
The gastro-intestinal tract represents the largest interface between the human body and its environment. It is a multilayer system composed of mucus and epithelial cells that establish and regulate barriers, while directly connecting to the immune system. This interface allows fluxes of water and nutriments and prevents from the entry of antigens and pathogens. Thus, it is the first line of defense. The regulation of the permeability occurs through the paracellular pathway, which is supported by the epithelial complex of junctional proteins. The gut microbiota also plays a key role in the regulation of the immune and metabolic systems and also, in the protection against pathogens. The continuous cross-talks between the intestinal barrier and the microbiota are essential to maintain the intestinal integrity and therefore the global homeostasis in healthy conditions. Nowadays, most of the chronic syndromes and diseases, such as irritable bowel syndrome (IBS) but also metabolic or behavioral disorders, are associated with an increase of the gut permeability also called “leaky gut syndrome”. Indeed, the consequence of the hyperpermeability is a flow increase of water and nutriments across the intestinal barrier but also of pathogens or toxins, among others, promoting an immune response and inflammation. Many studies also associated changes in the gut microbiota composition, dysbiosis, with chronic diseases. The beneficial effects of probiotic strains are increasingly demonstrated from in vitro experimentations to clinical trials and these studies demonstrated that they can be used in both the prevention and treatment of these disorders. We aimed to better decipher the interactions between the intestinal epithelial components and the probiotic bacteria in the pathophysiological context of intestinal chronic disorders. To do that, we first designed an in vitro screening of over fifty strains, from different genus, based on trans-epithelial electrical resistance (TEER) of two types of human intestinal epithelial cell lines, Caco-2 and T84. With these models, six Lactobacillus strains were selected and we better characterized their probiotic properties (adhesion ability, biofilm stability, neurotransmitter production and enzyme activity). We further evaluated the effect of four of them in in vivo models of chronic low-grade inflammation and neonatal maternal separation using C57BL/6J mice. Finally, we determined the implication of the bacterial strains in the modulation of the gut permeability, through the study of the complex of cellular junctional proteins
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36

Schuster, Stephanie Ann Foley Joe Preston. "Electrokinetic chromatography using novel unilamellar vesicles for unique separations and prediction of intestinal permeability /." Philadelphia, Pa. : Drexel University, 2007. http://hdl.handle.net/1860/2579.

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37

Demirbas, Ucpinar Sibel. "Oligonucleotides and protease inhibitors transport across CaCo-2 cell monolayers-permeability effects of dimethylsulfoxide and citicholine /." Full text (PDF) from UMI/Dissertation Abstracts International, 2000. http://wwwlib.umi.com/cr/utexas/fullcit?p3004252.

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38

Zhou, Yi. "Mechanisms of S-nitrosothiols intestinal permeability and NO store formation within vascular wall to improve NO oral delivery systems." Thesis, Université de Lorraine, 2019. http://www.theses.fr/2019LORR0101/document.

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Les S-nitrosothiols (RSNO) comme le S-nitrosoglutathion (GSNO) sont des donneurs de monoxyde d’azote (NO) prometteurs pour le traitement des maladies cardiovasculaires. Cependant, ce sont des candidats médicaments peu stables. Précédemment, des nanoparticules chargées en GSNO (GSNO-NP) ont été incluses dans une matrice d’alginate/chitosan. Les particules composites ainsi produites avaient une bonne encapsulation et une libération prolongée de GSNO. De plus, leur administration orale à des rats produisait un stock de NO au niveau de la paroi de l’aorte. Elles avaient cependant plusieurs limitations : préparation et caractérisation longues, manque de stabilité et de reproductibilité. Ce travail avait donc trois objectifs : (1) déterminer le mécanisme d’absorption intestinale des RSNO non formulés ; (2) évaluer la capacité des RSNO non formulés à créer un stock vasculaire de NO ; 3) optimiser la formulation de GSNO. Nous avons montré, dans un modèle in vitro de barrière intestinale, que la perméabilité intestinale de GSNO, S-nitroso-N-acétylcystéine (NACNO) et S-nitroso-N-acetylpénicillamine (SNAP) se fait par un mécanisme passif, principalement par voie transcellulaire (également paracellulaire pour SNAP), avec une perméabilité moyenne. Après avoir traversé la barrière intestinale, les RSNO atteindront les vaisseaux sanguins. Pour comparer leur capacité à former un stock vasculaire de NO dans des aortes (avec endothélium intact ou retiré), nous avons quantifié le stock, vérifié sa biodisponibilité pour la vasorelaxation et évalué son impact sur une vasoconstriction induite par la phénylephrine (PHE). L’incubation des aortes avec les RSNO augmente le stock basal de NO par un facteur trois à cinq. Ce stock est mobilisable pour induire la vasorelaxation et efficace pour diminuer la réactivité vasculaire à la PHE (NACNO>GSNO = SNAP), seulement dans les aortes dont l’endothélium a été retiré. Comme la perméabilité intestinale des RSNO est moyenne, l’intégration du GSNO dans une formulation appropriée est nécessaire. Vu l’impossibilité de résoudre les problèmes liés aux particules composites, le protocole de production des GSNO-NP a été modifié pour produire des microparticules (deux types selon l’état liquide ou solide de GSNO dans la phase interne de l’émulsion). Les deux types de microparticules avaient une libération de GSNO ralentie par rapport aux GSNO-NP. Les nano- comme les micro-particules ont pu être stabilisées par lyophilisation, et amélioraient la perméabilité intestinale de GSNO (jusqu’à une forte perméabilité avec les microparticules). Par conséquent, une administration orale de nano/microparticules chargées en GSNO/RSNO pourrait représenter une nouvelle approche thérapeutique pour les maladies cardiovasculaires
S-nitrosothiols (RSNOs) such as S-nitrosoglutathione (GSNO) are promising nitric oxide (NO) donors for cardiovascular diseases treatment. However, they are poorly stable drug candidates. In previous studies, GSNO-loaded nanoparticles (GSNO-NP) were embedded into an alginate/chitosan matrix. Resulting nanocomposite particles showed high encapsulation and sustained release of GSNO, and led to the formation of a NO store in the wall of aorta after a single oral administration to rats. However, these nanocomposite particles have several limitations such as time-consuming preparation, lack of both stability and reproducibility. This thesis work aimed at: 1) Elucidate the mechanism of free RSNOs intestinal absorption; 2) Evaluate ability of free RSNOs to form a vascular NO store; 3) Optimize the GSNO formulation. In this study, we showed that the intestinal permeability (in vitro model of intestinal barrier) of GSNO, S-nitroso-N-acetylcysteine (NACNO) and S-nitroso-N-acetylpenicillamine (SNAP) was a passive diffusion, following the transcellular pathway (and also the paracellular way for SNAP) and belonging to the medium permeability class. After crossing the intestinal barrier, RSNOs will reach the vasculature. In order to compare the ability of free RSNOs to form a vascular store of NO either in endothelium-intact or endothelium-removed aortae, we quantified the store, verified its bioavailability for vasorelaxation and evaluated its impact on phenylephrine (PHE)-induced vasoconstriction. Incubation with RSNOs increased the basal NO store three to five times. This store is still bioavailable to induce vasorelaxation and efficient to induce vascular hyporeactivity to PHE (NACNO> GSNO = SNAP) only in endothelium-removed aortae. As intestinal permeability of RSNOs was in the medium class, the integration of GSNO into an appropriate delivery system is essential. Limitations of previously developed nanocomposites particles were impossible to bypass so the production process of GSNO-NP was modified (liquid or solid GSNO in the internal phase of the emulsion) to produce microparticles. Both kinds of microparticles exhibited a slower release of GSNO than GSNO-NP. Nano-and micro-particles were stable after lyophilization and presented an enhancement of GSNO intestinal permeability (up to high permeability class for microparticles). Thus, oral administration of GSNO/RSNO loaded nano/micro particles seems to be a promising avenue for the treatment of cardiovascular diseases
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39

Chucta, Emily E. "LC-PUFA and sialyllactose modulation of intestinal permeability and the inflammatory response when challenged in the porcine intestinal cell line IPEC-J2." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu156614954555964.

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40

Dossou-Yovo, Flore. "Modification de la biodisponibilité orale des médicaments : interactions « Herb-Drugs » « Drugs- Drugs»." Thesis, Paris, CNAM, 2014. http://www.theses.fr/2014CNAM0936/document.

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L’administration par voie orale des médicaments reste encore de nos jours la voie royale de la prise des médicaments car moins onéreuse et plus adaptée au confort du patient. Mais cette voie reste toujours inaccessible pour certains médicaments comme les médicaments biologiques et les bio similaires voir certains anticancéreux et antirétroviraux.Le but de ce travail est d’améliorer la biodisponibilité par voie orale des médicaments à faible biodisponibilité par la mise au point d’un promoteur d’absorption. Pour y arriver nous avons adopté comme stratégie de développer un promoteur qui agit à la fois sur le passage passif et sur le passage actif des médicaments. Les études in vitro ont été réalisées en chambre de perméation d’Ussing adaptées par la société Biomécatronics SAS (BéthuneFrance). Dans la première partie de ce travail (Brevet), nous avons montré que l’utilisation d’une composition pharmaceutique et/ou diététique comprenant un extrait de plante(Hibiscus sabdariffa) pouvait augmenter la biodisponibilité in vitro des médicaments et des xénobiotiques qui passent par la voie paracellulaire comme le cisplatine (21 fois),l’oxaliplatine (11fois), la fluorescéine isothiocyanate-Dextran 4000 (3 fois), mais également les médicaments connus pour leur transport actif par la voie transcellulaire comme l’Efavirenz (7 fois) et l’Atazanavir (4 fois). Dans la seconde partie de ce travail, nous avons cherché à vérifier si notre promoteur d’absorption des médicaments a un effet sur la couche de mucus intestinale.Cette couche peut être un facteur limitant de passage des médicaments au travers de la barrière intestinale.Dans un premier temps (article 1), nous avons induit l’augmentation de la couche mucus au niveau du colon de rat après un prétraitement pendant une semaine avec le métronidazole. Puis nous avions confirmé (article 2) que l’administration par voie orale de deux antibiotiques le Cotrimoxazole (CTX) et le métronidazole (MTZ) pendant une semaine augmente la couche de mucus au niveau du côlon ; aussi nous avons montré qu’il existe une relation entre l’augmentation de la couche de mucus et la diminution de la conductance qui est l’index de transport passif des ions, des électrolytes et de certaines molécules à faibles poids moléculaires.De plus l’augmentation de la couche de mucus au niveau de l’intestin est responsable de la diminution du passage transépithélial des deux antirétroviraux dont l’utilisation est recommandée en première ligne par l’OMS (le.Ritonavir et l’Atazanavir) surles sujets porteurs du VIH (virus de l’immunodéficience humain). Après les traitements auMTZ et au CTX la sécrétion de l’Atazanavir augmente respectivement dans le côlon proximal de 2 et 4 fois et dans le côlon distal de 3 et 5 fois. On obtient également une sécrétion du Ritonavir de 5 et 10 fois dans le proximal et de 2 et 5 fois plus dans le distal.Le travail se poursuit par l’étude de l’effet de notre promoteur d’absorption des médicaments sur la couche de mucus intestinal.En conclusion, ce travail montre que l’on peut augmenter la biodisponibilité in vitroen utilisant les promoteurs de l’absorption des xénobiotiques qui agissent à la fois au niveau du transport passif et actif
Oral dosing is still seen as the silver bullet of drug administration, as it is cheaper andbetter adapted to patient comfort. However, oral route is still inaccessible to many drugssuch as biologics and biosimilars respectively certain anticancer drugs and antiretrovirals(ARV).The aim of this present study was to find new drugs enhancers that improve the oralbioavailability of drugs and xenobiotics. All the studies were realized in vitro using Ussingchambers technic. To achieve the set objective we used the strategy to develop drugenhancer which can modulate at the same time transcellular and paracellular pathways.In the first part of this study (patent) we have shown that the use of a pharmaceutical and /or a dietetic formulation containing a plant extract (Hibiscus sabdariffa) could increase thebioavailability in vitro in rats not only of cisplatin (21 fold), oxaliplatin (11 fold) andFluorescein Isothiocyanate-Dextran 4000 (FD4, 3 fold). All that drugs were transportedthrough intestinal barrier using paracellular pathway. In addition the study showed thatthis formulated enhancer can increased the bioavailability of Efavirenz (7 fold) andAtazanavir (4 fold) which are active transported.In order to assess the effect of new drugs enhancer on mucus thickness that limits thetransport of xenobiotic through intestinal barrier, we decide to evaluate his effect on passiveand active transport of drugs.In the second part of this study we have shown that after a week of pre-treatment of ratswith Metronidazole (MTZ, publication 1) and Cotrimoxazole (CTX, publication 2), the twomost commonly used antibiotics in the prophylaxis against opportunistic infections in HIV /AIDS, both increase colonic mucus thickness that affect directly passive intestinalpermeability by reducing conductance an index of passive transport through intestinalepithelium. In addition those antibiotics also entail a change in the transepithelialconductance and ARV fluxes. After MTZ and CTX treatment the secretion of Atazanavir(ATZ) increases respectively in the proximal colon by 2 to 4 fold and in the distal colon by 3to 5 fold respectively. Ritonavir (RTV) is poorly absorbed in control, after a week of pretreatmentwith MTZ and CTX one rather notices a secretion of RTV 5 to 10 fold higher in theproximal and 2 to 5 fold higher in the distal colon. The next study will be conducted toevaluate the effect of new drugs enhancer on mucus thickness layer.In conclusion, oral bioavailability of drugs and xenobiotics can be enhanced bypharmaceutical composition that contains herbal extract which increase passive and activetransport of drugs through intestinal barrier
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41

Denizot, Jérémy. "Perméabilité intestinale et régulation de l'expression du gène CEACAM6 : implication des bactéries Escherichia coli associées à la maladie de Crohn." Thesis, Clermont-Ferrand 1, 2013. http://www.theses.fr/2013CLF1MM04/document.

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La maladie de Crohn (MC) est une maladie inflammatoire chronique du tube digestif caractérisée par un état d'hyperactivation du système immunitaire intestinal et évoluant par poussées aigües entrecoupées de périodes de rémission. Les données cliniques et expérimentales montrent que l'étiologie de la MC serait une réponse immunitaire aberrante en réponse à des facteurs environnementaux tels que la consommation de nourriture riche en graisses et en sucres, et infectieux chez un hôte génétiquement prédisposé. Les patients atteints de MC présentent une perméabilité intestinale anormalement élevée, pouvant expliquer la stimulation du système immunitaire intestinal par des bactéries et antigènes de la flore intestinale. La muqueuse iléale des patients atteints de MC est anormalement colonisée par des souches de Escherichia coli ayant la propriété d'adhérer et d'envahir les cellules épithéliales intestinales, de survivre et de se multiplier dans les macrophages en entraînant la sécrétion de TNF-α (Tumor Necrosis factor-alpha). Un pathovar de E. coli associé à la MC et dénommé AIEC pour "Adherent-Invasive E. coli" a été défini. Les souches AIEC utilisent, pour adhérer, la molécule CEACAM6, anormalement exprimée au niveau de l'épithélium iléal des patients atteints de MC. Le travail présenté dans ce document a permis de mettre en évidence la capacité des bactéries AIEC à altérer la fonction de barrière de l'épithélium intestinal dans un modèle de souris transgénique exprimant le récepteur CEACAM6 humain. Cette altération est associée à une forte induction de l'expression de la protéine de jonction Claudine-2, comme observé chez les patients atteints de MC. Une 2ème étude a mis en évidence qu'un régime alimentaire de type occidental entraîne une modification de la composition de la flore intestinale chez les souris CEABAC10 aboutissant à l'apparition d'un micro-environnement inflammatoire favorisant l'implantation des bactéries AIEC et le développement d'inflammation. Enfin, la dernière étude met en évidence les mécanismes de régulation de l'expression du gène CEACAM6 par le facteur de transcription HIF-1 (Hypoxia Inductible Factor-1), de façon dépendante de la méthylation de l'ADN. L'ensemble de ces travaux a permis de mettre en évidence les conséquences d'une infection par les bactéries AIEC et d'un régime de type occidental sur la fonction de barrière intestinale
No abstract available
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42

Jugan, Maria Christine. "Effects of Akkermansia muciniphila Supplementation on Markers of Intestinal Permeability in Dogs Following Antibiotic Treatment." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488318772663017.

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43

Groschwitz, Katherine R. "Mast cell-mediated intestinal barrier function in homeostasis and disease." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1291389792.

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44

FINCK, CAROLE. "Exploration de la permeabilite intestinale au cr 51-edta au cours des eczemas : notre experience a propos de 47 cas." Besançon, 1993. http://www.theses.fr/1993BESA3058.

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45

Allen, Hilary Kaye. "The Effects of Enteropathogenic and Commensal Escherichia coli on Tight Junction Permeability." Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1341611861.

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46

Le, Nga Thi Thanh. "Regulation of Intestinal Epithelial Barrier and Immune Function by Activated T Cells." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1599833768774075.

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47

Juel, Ingebjørg S. "Intestinal injury and recovery after ishemia - An experimental study on restitution of the surface epithelium, intestinal permeability, and release of biomarkers from the mucosa." Doctoral thesis, Norwegian University of Science and Technology, Department of Cancer Research and Molecular Medicine, 2007. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-1817.

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48

Edrees, W. K. "The effect of lower limb ischaemia-reperfusion injury on intestinal permeability and the systemic inflammatory response." Thesis, Queen's University Belfast, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391116.

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49

McGilligan, Victoria. "The protective mechanisms of nicotine in relation to intestinal epithelial permeability and inflammation in ulcerative colitis." Thesis, University of Ulster, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.445045.

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50

Freitas, Antonio Klingem Leite de. "Efeito da SuplementaÃÃo com Alanil-Glutamina nas AlteraÃÃes da Permeabilidade Intestinal em Ratos Treinados Submetidos a um ExercÃcio Prolongado e Exaustivo de NataÃÃo." Universidade Federal do CearÃ, 2013. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=12375.

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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico
O exercÃcio prolongado e exaustivo induz uma disfunÃÃo da barreira intestinal. VÃrios estudos mostram que a suplementaÃÃo com alanil-glutamina (A/G) melhora a proliferaÃÃo das cÃlulas intestinais e absorÃÃo de eletrÃlitos. O objetivo deste trabalho foi investigar o efeito da suplementaÃÃo com A/G na permeabilidade intestinal em ratos treinados apÃs um exercÃcio prolongado e exaustivo de nataÃÃo. Utilizamos ratos Wistar, divididos em sete grupos: 1) SedentÃrio (S); 2) SedentÃrio A/G (S-A/G); 3) Treinado (T); 4) Treinado A/G (T-A/G); 5) ExaustÃo (E); 6) ExaustÃo A/G (E-A/G) e 7) Recuperado (R). Os animais dos grupos suplementados receberam o dipeptÃdeo A/G. Os animais foram treinados durante 12 semanas de nataÃÃo. Na metodologia realizamos anÃlises bioquÃmicas de pH, pCO2, pO2, SO2, excesso de bases (BE), pelo mÃtodo de gasometria e lactato e glicose. Analisamos a transcriÃÃo das junÃÃes firmes: ZO-1, Ocludina, Claudina-2 e PEPT-1 atravÃs de RT-PCR. A anÃlise da permeabilidade intestinal foi realizada pelo mÃtodo da ingestÃo de Lactulose/Manitol (L/M). Fizemos tambÃm anÃlise histolÃgica do duodeno, jejuno e Ãleo. O presente estudo foi aprovado pela CEPA-UFC, em protocolo de N 13/13. Nossos resultados mostraram que pCO2 e SO2 foram aumentados nos grupos E e E-A/G, mas houve queda nos parÃmetros de pH e BE para estes mesmos grupos. Encontramos queda dos Ãndices de glicose e aumento das concentraÃÃes de lactato. Houve aumento significativo no percentual de excreÃÃo de lactulose nos grupos E e E-A/G em relaÃÃo ao grupo S. Houve, no entanto, queda da excreÃÃo de lactulose com diferenÃa estatÃstica entre os grupos E e E-A/G, mostrando proteÃÃo da A/G frente ao aumento da permeabilidade intestinal promovida pelo exercÃcio exaustivo. O percentual de excreÃÃo do manitol foi aumentado nos grupos E e E-A/G em relaÃÃo ao grupo S. Entretanto, na anÃlise da relaÃÃo da permeabilidade dos dois carboidratos L/M observamos um aumento significativo no grupo E em relaÃÃo ao grupo S. Contudo, houve diferenÃa significativa entre os grupos E e E-A/G mostrando que a A/G conseguiu reverter os efeitos da atividade exaustiva na permeabilidade intestinal. Observamos aumento da ZO-1 e ocludina nos grupos S-A/G e T em relaÃÃo a S. Houve tambÃm aumento de ZO-1 no grupo E em relaÃÃo ao S. PorÃm, a A/G reverteu à transcriÃÃo destas junÃÃes firmes nos grupos T-A/G e E-A/G. A transcriÃÃo de claudina-2 foi reduzida no grupo S-A/G, mas obtivemos um aumento no grupo E em relaÃÃo ao S e uma diminuiÃÃo de E-A/G em relaÃÃo ao E. Em relaÃÃo ao PEPT-1, observamos aumento da transcriÃÃo nos grupos T e E em relaÃÃo ao S. Contudo, a A/G reverteu à transcriÃÃo deste peptÃdeo no grupo E-A/G em relaÃÃo ao E. Numa anÃlise de 72 horas apÃs o teste de exaustÃo encontramos valores para a permeabilidade intestinal similares aos grupos sedentÃrios. ConcluÃmos que o exercÃcio prolongado e exaustivo alterou a permeabilidade intestinal e a suplementaÃÃo crÃnica com alanil-glutamina teve efeito protetor contra este aumento. O possÃvel mecanismo da A/G no processo estudado refere-se a processos mecÃnicos de interaÃÃo cÃlula-cÃlula (ZO-1 e ocludina) e/ou eletrolÃticos (claudina-2).
The prolonged and exhaustive exercise induces intestinal barrier dysfunction. Several studies show that supplementation with alanyl-glutamine (A/G) improves the cell proliferation intestinal and electrolyte absorption. The aim of our study was to investigate the effect of supplementation with A/G in the intestinal permeability in rats trained after prolonged exercise and exhaustive swimming. We used Wistar rats that were divided into seven groups: 1) Sedentary (S); 2) Sedentary A/G (S-A/G); 3) Trained (T); 4) Trained A/G (T-A/G); 5) Exhaustion (E); 6) Exhaustion A/G (E-A/G); 7) Recovered (R). The animal supplemented groups received the dipeptide A/G. The animals were trained for twelve weeks. In the methodology we performed biochemical analysis of pH, pCO2, pO2, SO2, and bases excess (BE), by the method of gas analysis and lactate and glucose. We analyzed the transcription of tight junctions: ZO-1, Occludin, Claudin-2 and PEPT-1 by RT-PCR. The analysis of intestinal permeability was performed by the method of the ingestion of lactulose/mannitol (L/M). We also performed histological analysis of the duodenum, jejunum and ileum. This study was approved by the CEPA-UFC on Protocol NÂ 13/2013. Our results showed that SO2 and pCO2 were higher in groups E and E-A/G, but decreased the parameters pH and BE for these same groups. We found falling glucose levels and increased concentrations of lactate. A significant increase in the percentage of excretion of lactulose in groups E and E-A/G than in group S. There was, however, fall of excretion of lactulose with statistical difference between groups E and E-A/G, showing protection against the alanyl-glutamine increased intestinal permeability promoted by exhaustive exercise. The percentage of excretion of mannitol was increased in groups E and E-A/G than in group S. However, in the analysis of the excretion of both carbohydrates lactulose/mannitol we observed a significant increase in group E than in group S. However, there was significant difference between groups E and E-A/G showing that Ala/Gln was able to reverse the effects of exhaustive activity in intestinal permeability. We observed an increase in ZO-1 and occludin in groups S-A/G and T with respect to S. There was also an increase of ZO-1 in the E group compared to S. However, Ala/Gln reversed the transcription of these tight junctions in groups T-A/G and E-A/G. Transcription of claudin-2 was reduced in the S-A/G, but we obtained and increase in the E group compared to a decrease of S and E-A/G against E. Regarding the PET-1 we showed increased transcription in groups T and E in relation to S. However, the Ala/Gln reversed the transcript of this dipeptide in group E-A/G with respect to E. An analysis 72 hours after the exhaustion test values found for intestinal permeability similar to sedentary group. The prolonged and exhaustive exercise altered intestinal permeability and chronic supplementation with Ala/Gln was protective against the increase. The possible mechanism of Ala/Gln refers to mechanical processes of cell-to-cell interaction (occludin and ZO-1) and/or electrolytic (claudin-2).
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