Journal articles on the topic 'Permeabilità intestinale'
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Bottaccioli, Anna Giulia. "La malattia infiammatoria cronica intestinale: cure integrate in ottica Pnei." PNEI REVIEW, no. 2 (November 2020): 30–40. http://dx.doi.org/10.3280/pnei2020-002004.
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La malattia infiammatoria cronica intestinale (MICI) è una malattia idiopatica autoimmune che colpisce l'apparato digerente a causa dalla risposta immunitaria disregolata contro la microflora intestinale. I due principali tipi di MICI sono la rettocolite ulcerosa (RCU) e il morbo di Crohn (MC). Lo studio dell'asse intestino-cervello applicato alle MICI ha correlato lo stress con il peggioramento dell'attività di malattia. Durante lo stress, il cortisolo incrementa la permeabilità della barriera intestinale, favorendo la disbiosi intestinale e l'attivazione immunitaria in senso pro-infiammatorio. Un altro elemento osservato nelle MICI è l'alterazione del sistema neurovegetativo e in particolare la riduzione delle fibre efferenti vagali nel tratto digerente con conseguente fallimento del riflesso anti-infiammatorio vagale ed aumento dell'infiammazione. Vengono illustrate le evidenze scientifiche di approcci terapeutici non farmacologici integrati alla terapia standard delle MICI, come dieta anti-infiammatoria, pre- e probiotici, trapianto di microbiota fecale, fitoterapia, stimolazione nervosa vagale, agopuntura, terapie mente-corpo (meditazione, yoga e rilassamento) e psicoterapia.
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Bianchi, Alfio Ernesto, Antonio Maggi, and Riccardo Raddino. "Il microbiota intestinale, tra salute e malattia: un vero attore a due facce." CARDIOLOGIA AMBULATORIALE 30, no. 2 (October 14, 2021): 85–91. http://dx.doi.org/10.17473/1971-6818-2021-2-1.
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Il microbiota intestinale è un ecosistema batterico cha ha proprietà difensive per l’ospite ma che in particolari condizioni può produrre metaboliti tossici e dannosi per l’organismo. Metaboliti benefici sono gli acidi grassi a catena corta (SCAF), i metaboliti biliari ed i probiotici. Metaboliti dannosi sono la trimetilamina-N-ossidata (TMAO), i lipopolisaccaridi (LPS) e le tossine uremiche. La permeabilità della mucosa intestinale è la causa principale del passaggio in circolo di metaboliti dannosi. Il microbiota può intervenire in modo difensivo o dannoso in molte patologie cardiovascolari come la cardiopatia ischemica e lo scompenso ed in situazioni cliniche come il diabete, l’obesità, la malattia renale, la colite ulcerosa, il morbo di Chron e le malattie neurodegenerative. La dieta corretta è il cardine per mantenere una una favorevole funzionalità del microbiota.
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Bertossi, Francesca. "Il ruolo del microbiota nell'aumento ponderale associato alla terapia antipsicotica." PNEI REVIEW, no. 2 (November 2022): 108–22. http://dx.doi.org/10.3280/pnei2022-002010.
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Per il trattamento di un disturbo mentale severo e la prevenzione delle ricadute sono indicate delle terapie a lungo termine con farmaci antipsi- cotici. Gli antipsicotici di seconda generazione sono associati ad un minor numero di sintomi extrapiramidali, tuttavia sono gravati da importanti effetti collaterali di tipo metabolico e dal rischio di aumento ponderale, effetti mediati sia dai recettori centrali e periferici, sia a modifiche della composizione del microbiota. Numerose sono le evidenze del ruolo del microbiota intestinale nell'indur- re l'aumento ponderale ed i disturbi metabolici indotti dagli antipsicotici di seconda generazione attraverso un alterato segnale dello stimolo della fame e della sazietà, una riduzione della spesa energetica, la modulazione del metabolismo lipidico e glucidico, le modifiche dell'infiammazione e del- la permeabilità della barriera intestinale. Nella prevenzione e nel trattamento integrato dell'aumento ponderale as- sociato alla terapia antipsicotica, oltre alle terapie di tipo farmacologico, i programmi nutrizionali e l'attività fisica trova impiego un approccio volto a modulare il microbiota intestinale per correggere la disbiosi. Tra i diversi probiotici impiegati quello più promettente sembra essere l'Akkermansia muchiniphila.
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Pabla, D., F. Akhlaghi, H. Zia, Marco Centanni, and Nunzia Brusca. "Incremento della permeabilità intestinale alla levotiroxina sodica mediante acidi grassi a catena lineare studiata in linee di cellule epiteliali MDCK." L'Endocrinologo 12, no. 5 (October 2011): 259–60. http://dx.doi.org/10.1007/bf03344845.
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Cavin, Jean-Baptiste, Hailey Cuddihey, Wallace K. MacNaughton, and Keith A. Sharkey. "Acute regulation of intestinal ion transport and permeability in response to luminal nutrients: the role of the enteric nervous system." American Journal of Physiology-Gastrointestinal and Liver Physiology 318, no. 2 (February 1, 2020): G254—G264. http://dx.doi.org/10.1152/ajpgi.00186.2019.
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The small intestine regulates barrier function to absorb nutrients while avoiding the entry of potentially harmful substances or bacteria. Barrier function is dynamically regulated in part by the enteric nervous system (ENS). The role of the ENS in regulating barrier function in response to luminal nutrients is not well understood. We hypothesize that the ENS regulates intestinal permeability and ion flux in the small intestine in response to luminal nutrients. Segments of jejunum and ileum from mice were mounted in Ussing chambers. Transepithelial electrical resistance (TER), short-circuit current ( Isc), and permeability to 4-kDa FITC-dextran (FD4) were recorded after mucosal stimulation with either glucose, fructose, glutamine (10 mM), or 5% Intralipid. Mucosal lipopolysaccharide (1 mg/mL) was also studied. Enteric neurons were inhibited with tetrodotoxin (TTX; 0.5 μM) or activated with veratridine (10 μM). Enteric glia were inhibited with the connexin‐43 blocker Gap26 (20 μM). Glucose, glutamine, Intralipid, and veratridine acutely modified Isc in the jejunum and ileum, but the effect of nutrients on Isc was insensitive to TTX. TTX, Gap26, and veratridine treatment did not affect baseline TER or permeability. Intralipid acutely decreased permeability to FD4, while LPS increased it. TTX pretreatment abolished the effect of Intralipid and exacerbated the LPS‐induced increase in permeability. Luminal nutrients and enteric nerve activity both affect ion flux in the mouse small intestine acutely but independently of each other. Neither neuronal nor glial activity is required for the maintenance of baseline intestinal permeability; however, neuronal activity is essential for the acute regulation of intestinal permeability in response to luminal lipids and lipopolysaccharide. NEW & NOTEWORTHY Luminal nutrients and enteric nerve activity both affect ion transport in the mouse small intestine acutely, but independently of each other. Activation or inhibition of the enteric neurons does not affect intestinal permeability, but enteric neural activity is essential for the acute regulation of intestinal permeability in response to luminal lipids and lipopolysaccharide. The enteric nervous system regulates epithelial homeostasis in the small intestine in a time-dependent, region- and stimulus-specific manner.
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Dahlgren, David, Maria-Jose Cano-Cebrián, Tobias Olander, Mikael Hedeland, Markus Sjöblom, and Hans Lennernäs. "Regional Intestinal Drug Permeability and Effects of Permeation Enhancers in Rat." Pharmaceutics 12, no. 3 (March 8, 2020): 242. http://dx.doi.org/10.3390/pharmaceutics12030242.
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Sufficient colonic absorption is necessary for all systemically acting drugs in dosage forms that release the drug in the large intestine. Preclinically, colonic absorption is often investigated using the rat single-pass intestinal perfusion model. This model can determine intestinal permeability based on luminal drug disappearance, as well as the effect of permeation enhancers on drug permeability. However, it is uncertain how accurate the rat single-pass intestinal perfusion model predicts regional intestinal permeability and absorption in human. There is also a shortage of systematic in vivo investigations of the direct effect of permeation enhancers in the small and large intestine. In this rat single-pass intestinal perfusion study, the jejunal and colonic permeability of two low permeability drugs (atenolol and enalaprilat) and two high-permeability ones (ketoprofen and metoprolol) was determined based on plasma appearance. These values were compared to already available corresponding human data from a study conducted in our lab. The colonic effect of four permeation enhancers—sodium dodecyl sulfate, chitosan, ethylenediaminetetraacetic acid (EDTA), and caprate—on drug permeability and transport of chromium EDTA (an established clinical marker for intestinal barrier integrity) was determined. There was no difference in jejunal and colonic permeability determined from plasma appearance data of any of the four model drugs. This questions the validity of the rat single-pass intestinal perfusion model for predicting human regional intestinal permeability. It was also shown that the effect of permeation enhancers on drug permeability in the colon was similar to previously reported data from the rat jejunum, whereas the transport of chromium EDTA was significantly higher (p < 0.05) in the colon than in jejunum. Therefore, the use of permeation enhancers for increasing colonic drug permeability has greater risks than potential medical rewards, as indicated by the higher permeation of chromium EDTA compared to the drugs.
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Pijls, Kirsten E., Ger H. Koek, Elhaseen E. Elamin, Hanne de Vries, Ad A. M. Masclee, and Daisy M. A. E. Jonkers. "Large intestine permeability is increased in patients with compensated liver cirrhosis." American Journal of Physiology-Gastrointestinal and Liver Physiology 306, no. 2 (January 15, 2014): G147—G153. http://dx.doi.org/10.1152/ajpgi.00330.2013.
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Intestinal barrier dysfunction, facilitating translocation of bacteria and bacterial products, plays an important role in the pathophysiology of liver cirrhosis and its complications. Increased intestinal permeability has been found in patients with liver cirrhosis, but data on small and large intestine permeability and tight junctions (TJs) in patients with compensated cirrhosis are scarce. We aimed to investigate both small and large intestine permeability in patients with stable compensated cirrhosis compared with healthy controls and evaluated the expression of TJ proteins in mucosal biopsies at duodenal and sigmoid level. Intestinal permeability was assessed in 26 patients with compensated cirrhosis and 27 matched controls using a multisugar test. Duodenal and sigmoid biopsies were available from a subgroup for analyses of gene transcription and expression of key TJ proteins by qRT-PCR and ELISA, respectively. Median 0–5-h urinary sucrose excretion and lactulose/rhamnose ratio were comparable between patients with compensated cirrhosis and controls, whereas 5–24-h urinary sucralose/erythritol ratio was increased in these patients. Downregulation of gene transcription was found for claudin-3 in duodenal biopsies and claudin-4 in sigmoid biopsies, and at the protein level occludin expression was significantly increased in both duodenal and sigmoid biopsies. This study shows that gastroduodenal and small intestine permeability are not altered, whereas large intestine permeability is increased in patients with stable compensated cirrhosis. Only limited alterations were found regarding the expression of TJ proteins in both the small and large intestine.
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Markovic, Milica, Moran Zur, Sapir Garsiani, Daniel Porat, Sandra Cvijić, Gordon L. Amidon, and Arik Dahan. "The Role of Paracellular Transport in the Intestinal Absorption and Biopharmaceutical Characterization of Minoxidil." Pharmaceutics 14, no. 7 (June 27, 2022): 1360. http://dx.doi.org/10.3390/pharmaceutics14071360.
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The purpose of this study was to evaluate mechanisms behind the intestinal permeability of minoxidil, with special emphasis on paracellular transport, and elucidate the suitability of minoxidil to be a reference drug for Biopharmaceutics Classification System (BCS). The permeability of minoxidil (vs. metoprolol) was evaluated in-silico, in-vitro using both the PAMPA assay and across Caco-2 cell monolayers, as well as in-vivo in rats throughout the entire intestine. The permeability was studied in conditions that represent the different segments of the small intestine: upper jejunum (pH 6.5), mid small intestine (pH 7.0), distal ileum (pH 7.5), and colon (pH 6.5). Since we aimed to investigate the paracellular transport of minoxidil, we have also examined its permeability in the presence of quercetin (250 µM), which closes the tight junctions, and sodium decanoate (10 mM), which opens the tight junctions. While metoprolol demonstrated segmental-dependent rat and PAMPA permeability, with higher permeability in higher pH regions, the permeability of minoxidil was pH-independent. Minoxidil PAMPA permeability was significantly lower than its rat permeability, indicating a potential significant role of the paracellular route. In rat intestinal perfusion studies, and across Caco-2 monolayers, tight junction modifiers significantly affected minoxidil permeability; while the presence of quercetin caused decreased permeability, the presence of sodium decanoate caused an increase in minoxidil permeability. In accordance with these in-vitro and in-vivo results, in-silico simulations indicated that approximatelly 15% of minoxidil dose is absorbed paracellularly, mainly in the proximal parts of the intestine. The results of this study indicate that paracellular transport plays a significant role in the intestinal permeability of minoxidil following oral administration. Since this permeation route may lead to higher variability in comparison to transcellular, these findings diminish the suitability of minoxidil to serve as the low/high BSC permeability class benchmark.
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Willems, D., S. Cadranel, and W. Jacobs. "Measurement of urinary sugars by HPLC in the estimation of intestinal permeability: evaluation in pediatric clinical practice." Clinical Chemistry 39, no. 5 (May 1, 1993): 888–90. http://dx.doi.org/10.1093/clinchem/39.5.888.
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Abstract Determinations of the permeability of the intestine to various sugars have been used to assess intestinal mucosal abnormalities, but the widespread application of such tests has been prohibited by the complexity of most classically used techniques. In this study, we evaluated the sensitivity and practicability of using HPLC to estimate intestinal permeability, with mannitol and lactulose as mono- and disaccharides, respectively. The results of the permeability tests were compared with those of intestinal biopsy in 20 children. All patients with an abnormal intestinal biopsy showed a low mannitol recovery, and the patients with allergic symptoms showed a high lactulose recovery. Our preliminary data suggest that HPLC is reliable, gives results comparable with those of other methods, and is a practical way to determine intestinal permeability noninvasively.
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Oscarsson, Elin, Tim Lindberg, Kathrin S. Zeller, Malin Lindstedt, Daniel Agardh, Åsa Håkansson, and Karolina Östbring. "Changes in Intestinal Permeability Ex Vivo and Immune Cell Activation by Three Commonly Used Emulsifiers." Molecules 25, no. 24 (December 15, 2020): 5943. http://dx.doi.org/10.3390/molecules25245943.
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Food additives such as emulsifiers are used in increasing quantities in the food industry. The aim of this study was to compare three different emulsifiers (polysorbate 80 (P80), carboxymethyl cellulose (CMC), and β-lactoglobulin (β-lac) with regards to their effect on the stimulation of immune cells and intestinal permeability. The immune stimulatory effects were studied in the myeloid cell line MUTZ-3-cells, while the change in intestinal permeability was studied in the Caco-2 cell line and ex vivo in the Ussing chamber system using small intestinal fragments from rats. The tested concentrations of the emulsifiers ranged from 0.02% up to 1%, which are concentrations commonly used in the food industry. The results showed that P80 affected both the myeloid cells and the intestinal permeability more than CMC (p < 0.05) and β-lac (p < 0.05) at the highest concentration. CMC was found to neither affect the permeability in the intestine nor the MUTZ-3 cells, while β-lac changed the permeability in the total part of the small intestine in rats. These findings indicate that P80 might be more cytotoxic compared to the other two emulsifiers.
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Rabba, Abdullah Khalil, Luqin Si, Kewen Xue, Ming Li, and Gao Li. "In Situ Intestinal Perfusion of Irinotecan: Application to P-gp Mediated Drug Interaction and Introduction of an Improved HPLC Assay." Journal of Pharmacy & Pharmaceutical Sciences 14, no. 2 (April 18, 2011): 138. http://dx.doi.org/10.18433/j36w2j.
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PURPOSE: To determine experimentally the intestinal permeability of the anticancer prodrug irinotecan, and to quantify the amount of its cytotoxic metabolite SN-38 that is intestinally excreted (exsorped) as a predictor of intestinal toxicity, and to assess the effect of p-glycoprotein (p-gp) inhibitors (verapamil as a model) on the permeability and toxicity of irinotecan. METHODS: Single pass intestinal perfusion of rat’s whole length small intestines is applied to assess the permeability of the parent drug and quantify the intestinally excreted metabolite. The perfusion solution contained 30μg/ml of irinotecan (control group) without or with verapamil (verapamil group). A simple reversed phase HPLC method with UV detection is developed and validated for simultaneous determination of irinotecan and SN-38 using camptothecin as an internal standard. RESULTS: HPLC-UV method found to be simple, specific, accurate, and precise. Effective permeability coefficient of irinotecan found to be 4.9±1.7 10-3 mm/min and was doubled in verapamil group (P=0.007). Average cumulative amount of SN-38 exsorped found to be 29 ng/cm over 2 hours perfusion time which was decreased to 15 ng/cm in verapamil group (P=0.016). CONCLUSIONS: in situ intestinal perfusion method was successfully applied to quantify the permeability of irinotecan and the exsorption of SN-38 in the same experiment, in a manner that robustly reflects real in vivo situation. P-gp inhibition using verapamil found to significantly enhance the intestinal permeability of irinotecan and potentially decrease the intestinal toxicity due to SN-38 exposure.
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Hao, Yue, Yuejin Feng, Jielei Li, and Xianhong Gu. "Role of MAPKs in HSP70’s Protection against Heat Stress-Induced Injury in Rat Small Intestine." BioMed Research International 2018 (July 12, 2018): 1–10. http://dx.doi.org/10.1155/2018/1571406.
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Aim. To evaluate the role of heat shock protein 70 (HSP70) on the MAPK pathway activation with quercetin treatment and its protection against small intestine impairments of heat stressed rats. Methods. Forty-eight male Sprague-Dawley rats aged 6 weeks were randomized to three groups (n=16/group), namely, control (CON), heat stress (HS), and heat stress + quercetin (HQ). The experiment lasted for 14 days with daily 50 min of heat stress treatment (43°C) for the HS and HQ groups. Rats of HQ group were intragastrically given 0.5 ml quercetin solution (50 mg/kg body weight) before the heat stress treatment. Half of the animals were sacrificed on day 7 and the rest on day 14 for tissue sampling. Intestinal morphology, small intestine morphology and permeability, protein expression of HSP70, phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and caspase-3 activity were examined. Results. Heat stress caused morphological damage to the small intestine and increased intestinal permeability. HSP70 expression and MAPK activity in the small intestine were increased by heat stress. Inhibition of HSP70 by quercetin did not change intestinal permeability compared with the HS group but aggravated intestinal injury and affected the activation of MAPKs and caspase-3. Conclusions. HSP70 may modulate stress-activated signaling and acts in a protective manner via MAPK signaling. Affecting HSP70 protective mechanisms could be useful for protection against heat stress-induced injury in rat small intestine.
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Perry, M. A., A. P. Shepherd, P. R. Kvietys, and D. N. Granger. "Effect of hypoxia on feline intestinal capillary permeability." American Journal of Physiology-Gastrointestinal and Liver Physiology 248, no. 3 (March 1, 1985): G272—G276. http://dx.doi.org/10.1152/ajpgi.1985.248.3.g272.
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The multiple-indicator dilution technique was used to investigate the permeability characteristics of capillaries in the cat small intestine during hypoxia. Reducing the arterial oxygen tension from 108 to 35 mmHg for 10 min increased the calculated equivalent pore radius of intestinal capillaries from 59 to 67 A. This effect was sustained for at least 15 min after the hypoxic episode. Hypoxia did not alter intestinal lymphatic protein clearance. Thus, the dimensions of the large pores did not change. This study demonstrates that 10 min of severe hypoxia increases vascular permeability in the small intestine and that this change occurs only in the small pores and is sustained, at least briefly, after restoration of normoxia. Hypoxia does not significantly change the permeability to macromolecules.
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Shil, Aparna, Oluwatobi Olusanya, Zaynub Ghufoor, Benjamin Forson, Joanne Marks, and Havovi Chichger. "Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3." Nutrients 12, no. 6 (June 22, 2020): 1862. http://dx.doi.org/10.3390/nu12061862.
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The breakdown of the intestinal epithelial barrier and subsequent increase in intestinal permeability can lead to systemic inflammatory diseases and multiple-organ failure. Nutrition impacts the intestinal barrier, with dietary components such as gluten increasing permeability. Artificial sweeteners are increasingly consumed by the general public in a range of foods and drinks. The sweet taste receptor (T1R3) is activated by artificial sweeteners and has been identified in the intestine to play a role in incretin release and glucose transport; however, T1R3 has not been previously linked to intestinal permeability. Here, the intestinal epithelial cell line, Caco-2, was used to study the effect of commonly-consumed artificial sweeteners, sucralose, aspartame and saccharin, on permeability. At high concentrations, aspartame and saccharin were found to induce apoptosis and cell death in intestinal epithelial cells, while at low concentrations, sucralose and aspartame increased epithelial barrier permeability and down-regulated claudin 3 at the cell surface. T1R3 knockdown was found to attenuate these effects of artificial sweeteners. Aspartame induced reactive oxygen species (ROS) production to cause permeability and claudin 3 internalization, while sweetener-induced permeability and oxidative stress was rescued by the overexpression of claudin 3. Taken together, our findings demonstrate that the artificial sweeteners sucralose, aspartame, and saccharin exert a range of negative effects on the intestinal epithelium through the sweet taste receptor T1R3.
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Wan Saudi, Wan Salman, Md Abdul Halim, Tobias Rudholm-Feldreich, Linda Gillberg, Evelina Rosenqvist, Anders Tengholm, Magnus Sundbom, et al. "Neuropeptide S inhibits gastrointestinal motility and increases mucosal permeability through nitric oxide." American Journal of Physiology-Gastrointestinal and Liver Physiology 309, no. 8 (October 15, 2015): G625—G634. http://dx.doi.org/10.1152/ajpgi.00104.2015.
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Neuropeptide S (NPS) receptor (NPSR1) polymorphisms are associated with enteral dysmotility and inflammatory bowel disease (IBD). This study investigated the role of NPS in conjunction with nitrergic mechanisms in the regulation of intestinal motility and mucosal permeability. In rats, small intestinal myoelectric activity and luminal pressure changes in small intestine and colon, along with duodenal permeability, were studied. In human intestine, NPS and NPSR1 were localized by immunostaining. Pre- and postprandial plasma NPS was measured by ELISA in healthy and active IBD humans. Effects and mechanisms of NPS were studied in human intestinal muscle strips. In rats, NPS 100-4,000 pmol·kg−1·min−1 had effects on the small intestine and colon. Low doses of NPS increased myoelectric spiking ( P < 0.05). Higher doses reduced spiking and prolonged the cycle length of the migrating myoelectric complex, reduced intraluminal pressures ( P < 0.05-0.01), and increased permeability ( P < 0.01) through NO-dependent mechanisms. In human intestine, NPS localized at myenteric nerve cell bodies and fibers. NPSR1 was confined to nerve cell bodies. Circulating NPS in humans was tenfold below the ∼0.3 nmol/l dissociation constant ( Kd) of NPSR1, with no difference between healthy and IBD subjects. In human intestinal muscle strips precontracted by bethanechol, NPS 1–1,000 nmol/l induced NO-dependent muscle relaxation ( P < 0.05) that was sensitive also to tetrodotoxin ( P < 0.01). In conclusion, NPS inhibits motility and increases permeability in neurocrine fashion acting through NO in the myenteric plexus in rats and humans. Aberrant signaling and upregulation of NPSR1 could potentially exacerbate dysmotility and hyperpermeability by local mechanisms in gastrointestinal functional and inflammatory reactions.
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Vasileva, A. V., A. A. Morozov, S. V. Matrosova, N. A. Chechkova, M. V. Arnautov, R. V. Artemov, S. V. Bindyukov, A. V. Zhidko, and I. V. Sukhovskaya. "The effect of a high-protein and high-carbohydrate diet on the content of D-lactate in the blood plasma and intestines of a model organism – rainbow trout." Acta Biomedica Scientifica 7, no. 5-2 (December 11, 2022): 247–58. http://dx.doi.org/10.29413/abs.2022-7.5-2.25.
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D-lactic acid stereoisomer (D-lactate) is produced by the intestinal microflora and can enter the bloodstream and cause in some cases a condition of acute D-lactic acidemia known as short gut syndrome. The level of D-lactate in blood and in the contents of the intestine is considered as a promising marker of the development of inflammation associated with microflora disorders, as well as with the development of a bacterial infection, while the mechanism of its entry into the blood of vertebrates from the intestine has not been studied in detail.The aim of the study. To investigate the relationship between the level of D-lactate in blood and in the intestine, taking into account the permeability of the intestinal epithelium.Materials and methods. As a model object of the study, we used juvenile rainbow trout O. mykiss. For 54 days, they were high-carbohydrate or high-protein fed. Since different types of bacteria prefer different substrates, it was expected that at the end of the experiment, the composition of the intestinal microflora would be significantly different in fish fed with different diets. The content of D-lactate in blood plasma in vitro was assessed by the Larsen method with modifications; intestinal permeability was assessed by the intensity of fluorescence of the FITС-Dextran stain in the blood of fish. The analysis of the metagenome of samples of the contents and epithelium of the fore and hind intestine was carried out. The hematological profile was partially characterized using blood smears taken immediately after fish blood sampling. By the means of a different diet, it was possible to obtain two groups of fish that differ significantly in the permeability of the intestinal epithelium and in the content of D-lactate in the intestine. At the same time, despite the differences between the experimental groups in the content of D-lactate in the intestine and in intestinal permeability, no significant differences in D-lactate level in blood were found between them. Analysis of the composition of the intestinal microbiome by metabarcoding for the 16S rRNA gene revealed the absence of lactobacilli in the production of D-lactate in fish.Results. It was shown that the mechanism of accumulation of D-lactate in the blood plasma in fish is less associated with increased intestinal permeability or hyperproduction of this metabolite by the intestinal microflora and is more associated with the utilization of D-lactate in the body. In the experiment, it was not possible to achieve a significant change in the species composition of the intestinal microflora of trout under the influence of a highcarbohydrate diet for 54 days compared to fish that received high-protein diet. Some tendencies towards changes in the composition of the microflora were found in the contents of the hindgut, and perhaps with a longer exposure, these changes could reach a statistically significant level.
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Lambert, G. P., C. V. Gisolfi, D. J. Berg, P. L. Moseley, L. W. Oberley, and K. C. Kregel. "Selected Contribution: Hyperthermia-induced intestinal permeability and the role of oxidative and nitrosative stress." Journal of Applied Physiology 92, no. 4 (April 1, 2002): 1750–61. http://dx.doi.org/10.1152/japplphysiol.00787.2001.
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The purpose of this study was to characterize intestinal permeability changes over a range of physiologically relevant body temperatures in vivo and in vitro. Initially, FITC-dextran (4,000 Da), a large fluorescent molecule, was loaded into the small intestine of anesthetized rats. The rats were then maintained at ∼37°C or heated over 90 min to a core body temperature of ∼41, ∼41.5, or ∼42.5°C. Permeability was greater in the 42.5°C group compared with the 37, 41, or 41.5°C groups. Histological analysis revealed intestinal epithelial damage in heated groups. Everted intestinal sacs were then used to further characterize hyperthermia-induced intestinal permeability and to study the potential role of oxidative and nitrosative stress. Increased permeability to 4,000-Da FITC-dextran in both small intestinal and colonic sacs was observed at a temperature of 41.5–42°C compared with 37°C, along with widespread intestinal epithelial damage. Administration of antioxidant enzyme mimics or a nitric oxide synthase inhibitor did not reduce permeability due to heat stress, and tissue concentrations of a lipid peroxidation product were not altered by heat stress, suggesting that oxidative and nitrosative stress were not likely mediators of this phenomenon in vitro. In conclusion, hyperthermia produced increased permeability and marked intestinal epithelial damage both in vivo and in vitro, suggesting that thermal disruption of epithelial membranes contributes to the intestinal barrier dysfunction manifested with heat stress.
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Nakanishi, Takashi, Hirokazu Fukui, Xuan Wang, Shin Nishiumi, Haruka Yokota, Yutaka Makizaki, Yoshiki Tanaka, et al. "Effect of a High-Fat Diet on the Small-Intestinal Environment and Mucosal Integrity in the Gut-Liver Axis." Cells 10, no. 11 (November 14, 2021): 3168. http://dx.doi.org/10.3390/cells10113168.
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Although high-fat diet (HFD)-related dysbiosis is involved in the development of steatohepatitis, its pathophysiology especially in the small intestine remains unclear. We comprehensively investigated not only the liver pathology but also the microbiome profile, mucosal integrity and luminal environment in the small intestine of mice with HFD-induced obesity. C57BL/6J mice were fed either a normal diet or an HFD, and their small-intestinal contents were subjected to microbial 16S rDNA analysis. Intestinal mucosal permeability was evaluated by FITC-dextran assay. The levels of bile acids in the small-intestinal contents were measured by liquid chromatography/mass spectrometry. The expression of tight junction molecules, antimicrobial peptides, lipopolysaccharide and macrophage marker F4/80 in the small intestine and/or liver was examined by real-time RT-PCR and immunohistochemistry. The abundance of Lactobacillus was markedly increased and that of Clostridium was drastically decreased in the small intestine of mice fed the HFD. The level of conjugated taurocholic acid was significantly increased and those of deconjugated cholic acid/secondary bile acids were conversely decreased in the small-intestinal contents. The expression of occludin, antimicrobial Reg IIIβ/γ and IL-22 was significantly decreased in the small intestine of HFD-fed mice, and the intestinal permeability was significantly accelerated. Infiltration of lipopolysaccharide was significantly increased in not only the small-intestinal mucosa but also the liver of HFD-fed mice, and fat drops were apparently accumulated in the liver. Pathophysiological alteration of the luminal environment in the small intestine resulting from a HFD is closely associated with minimal inflammation involving the gut-liver axis through disturbance of small-intestinal mucosal integrity.
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Pinker, Elisha, and Timur Tuganbaev. "Microbiome Composition and Circadian Rhythm Disruption Alters Epithelial Barrier Integrity." Columbia Undergraduate Science Journal 15 (May 24, 2021): 6–15. http://dx.doi.org/10.52214/cusj.v15i1.7408.
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The intestine is home to one of the most complex ecological communities, termed the human gut microbiome. The gut microbiome modulates a wide range of human diseases from diabetes to neurological disorders to cancer. Separating the host and the gut microbiome is the epithelial barrier. The intestinal epithelium serves as an adaptive interaction hub between the host and microbiome that plays an important role in deciding the outcome of host-microbiome interactions. Regulation of epithelial barrier permeability to ions, nutrients and microbiome metabolites is known to be a tightly controlled process on the host side. However, whether the microbiome community also affects epithelial permeability remains unclear. Here, we show that alterations in microbiota composition by treatment with antibiotics selectively targeting specific members of the microbiome community impacts the permeability of the intestine. Additionally, modulating the microbiome through other methods such as altering diet composition shows changes in permeability of the epithelial barrier. As daily feeding rhythm entrains diurnal fluctuations in microbiome, we have set out to measure epithelial barrier permeability throw out the clock. We have discovered that the permeability of the intestinal epithelial barrier exhibits circadian rhythms in mice. Disruption of these rhythms, through jet-lag or genetic deficiencies in circadian machinery, consequently alters epithelial barrier integrity. Together, these findings provide evidence that disruptions in circadian rhythms as well as alterations in microbiome composition have direct consequences in intestinal permeability, and that microbiome might serve as a tool in regulating epithelium permeability.
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Mitchell, Samuel, Tolunay Aydemir, and Trista Thorn. "High Sucrose Diet Induces Intestinal Zinc Dyshomeostasis and Permeability." Current Developments in Nutrition 6, Supplement_1 (June 2022): 1191. http://dx.doi.org/10.1093/cdn/nzac074.020.
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Abstract Objectives Zinc (Zn) is an essential micronutrient that is critical for many physiological processes including glucose metabolism, regulation of inflammation, regulation of intestinal barrier function, and insulin production and secretion. Further, Zn dysregulation is associated with increased risk of chronic inflammatory diseases such as type II diabetes, inflammatory bowel disease, and obesity. However, it remains unclear whether altered Zn status is a symptom or cause of disease onset. Common symptoms of these three inflammatory diseases include the onset of intestinal inflammation and increased intestinal permeability. The specific focus of this work is to investigate how dietary sources of chronic inflammation, such as high sucrose consumption impacts transporter mediated Zn homeostasis and subsequent Zn dependent physiology. Methods To study the interactions between high dietary sucrose and Zn homeostasis, we administered 30% sucrose water to mice for 8 weeks. Tissue metal contents were measured by microwave plasma atomic emission spectrometry. Zn transport was measured using radioisotope tracing of 65Zn. Intestine permeability was assessed by FITC-dextran (4 kDa) assay. Protein expression of Zn transporters, inflammatory markers, and tight junction proteins was measured by western blot. Results Sucrose treatment resulted in systemic changes in steady-state Zn distribution, including a significant increase in plasma Zn and significant decreases in Zn in the liver, pancreas, and white adipose tissue. We observed changes in Zn transport protein expression in the intestine. In agreement with altered transporter expression, Zn transport studies revealed significant dysregulation of Zn transport in both the small intestine and colon. Further, sucrose treatment resulted in induction of both P-STAT3 and P-NF-κB, dysregulation of tight junction proteins ZO-1 and CLDN1, and increased intestine permeability. Conclusions Our work suggests that chronic high sucrose consumption leads to changes in systemic Zn homeostasis. This links diet-induced changes in Zn homeostasis to the onset of precursors of chronic disease, intestinal inflammation and permeability. Funding Sources This work was supported by Cornell University Division of Nutritional Sciences funds to T. B. Aydemir.
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Eremina, E. Yu. "Gastrointestinal symptoms in SARS-CoV‑2 infected: emphasis on increased mucosal permeability." Medical alphabet, no. 20 (August 18, 2021): 13–20. http://dx.doi.org/10.33667/2078-5631-2021-20-13-20.
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The article presents data on the prevalence of gastrointestinal symptoms in patients with COVID‑19, the mechanisms of its development, the impact on the course of the disease and the tactics of drug therapy. It is noted that the persistence of the SARS-CoV‑2 virus in the intestine may be responsible for an increase in the duration of the disease and the development of multi-organ lesions, since the intestine, on the one hand, is the site of penetration and replication of the SARS-CoV‑2 virus, and on the other, is a potential source of virus spread due to increased intestinal permeability against the background of infection and disturbed microbiocenosis. Based on this, it seems pathogenetically justified to use drugs in the complex therapy of patients that contribute to the normalization of intestinal microbiocenosis and intestinal permeability.
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Al-Sadi, Rana, Khaldun Khatib, Shuhong Guo, Dongmei Ye, Moustafa Youssef, and Thomas Ma. "Occludin regulates macromolecule flux across the intestinal epithelial tight junction barrier." American Journal of Physiology-Gastrointestinal and Liver Physiology 300, no. 6 (June 2011): G1054—G1064. http://dx.doi.org/10.1152/ajpgi.00055.2011.
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Defective intestinal epithelial tight junction (TJ) barrier has been shown to be an important pathogenic factor contributing to the development of intestinal inflammation. The expression of occludin is markedly decreased in intestinal permeability disorders, including in Crohn's disease, ulcerative colitis, and celiac disease, suggesting that the decrease in occludin expression may play a role in the increase in intestinal permeability. The purpose of this study was to delineate the involvement of occludin in intestinal epithelial TJ barrier by selective knock down of occludin in in vitro (filter-grown Caco-2 monolayers) and in vivo (recycling perfusion of mouse intestine) intestinal epithelial models. Our results indicated that occludin small-interfering RNA (siRNA) transfection causes an increase in transepithelial flux of various-sized probes, including urea, mannitol, inulin, and dextran, across the Caco-2 monolayers, without affecting the transepithelial resistance. The increase in relative flux rate was progressively greater for larger-sized probes, indicating that occludin depletion has the greatest effect on the flux of large macromolecules. siRNA-induced knock down of occludin in mouse intestine in vivo also caused an increase in intestinal permeability to dextran but did not affect intestinal tissue transepithelial resistance. In conclusion, these results show for the first time that occludin depletion in intestinal epithelial cells in vitro and in vivo leads to a selective or preferential increase in macromolecule flux, suggesting that occludin plays a crucial role in the maintenance of TJ barrier through the large-channel TJ pathway, the pathway responsible for the macromolecule flux.
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Kanno, Takuya, Takahito Katano, Isamu Ogawa, Takahiro Iwao, Tamihide Matsunaga, and Hiromi Kataoka. "Protective Effect of Irsogladine against Aspirin-Induced Mucosal Injury in Human Induced Pluripotent Stem Cell-Derived Small Intestine." Medicina 59, no. 1 (December 31, 2022): 92. http://dx.doi.org/10.3390/medicina59010092.
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Background and Objectives: Acetylsalicylic acid (ASA) is widely used for preventing cerebrovascular and cardiovascular diseases. Gastrointestinal (GI) tract injury is one of the major complications of aspirin use, potentially leading to severe GI bleeding. However, no drugs for preventing aspirin-induced small intestinal injury have been developed. The aim of this study was to establish a human experimental model for investigating aspirin-induced small intestinal mucosal injury. In addition, we evaluated the protective effect of Irsogladine against aspirin-induced small intestinal mucosal injury using human induced pluripotent stem cell-derived 2D monolayer crypt-villus structural small intestine (2D-hiPSC-SI). Materials and Methods: Human iPS cell-derived intestinal organoids were seeded and cultured in Air-liquid interface. The permeability of 2D-hiPSC-SI was evaluated using Lucifer yellow. Changes in structure and mucosal permeability of 2D-hiPSC-SI after addition of aspirin were confirmed over time, and changes in intestinal epithelium-related markers were evaluated by real-time qPCR and Immunofluorescence staining. The effect of Irsogladine on prevention of aspirin mucosal injury was examined by adding Irsogladine to the culture medium. Results: Cultured 2D-hiPSC-SI showed multi-lineage differentiation into small intestinal epithelium comprised of absorptive cells, goblet cells, enteroendocrine cells, and Paneth cells, which express CD10, MUC2, chromogranin A, and lysozyme, respectively. RNA in situ hybridization revealed intestinal stem cells that express Lgr5. ASA administration induced an increase in the mucosal permeability of 2D-hiPSC-SI. ASA-injured 2D-hiPSC-SI showed decreased mRNA expression of multi-lineage small intestinal cell markers as well as intestinal stem cell marker Lgr5. Administration of Irsogladine on the basal side of the 2D-hiPSC-SI resulted in significant increases in Mki67 and Muc2 mRNA expression by 2D-hiPSCs at 48 h compared with the control group. Administration of 400 µg/mL Irsogladine to the ASA-induced small intestinal injury model resulting in significantly decreased mucosal permeability of 2D-hiPSC-SI. In immunofluorescence staining, Irsogladine significantly increased the fluorescence intensity of MUC2 under normal conditions and administration of 400 µg/mL ASA. Conclusions: we established a novel ASA-induced small intestinal injury model using human iPSC-derived small intestine. Irsogladine maintains mucosal permeability and goblet cell differentiation against ASA-induced small intestinal injury.
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Gridnyev, O. Y., G. D. Fadieienko, I. E. Kushnir, and S. V. Gridnieva. "Intestinal permeability and its role in the pathogenesis and progress of non-alcoholic fatty liver disease. Review." Modern Gastroenterology, no. 1 (February 27, 2023): 55–67. http://dx.doi.org/10.30978/mg-2023-1-55.
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Non‑alcoholic fatty liver disease (NAFLD) is a topical problem for the medicine worldwide, and its association with an «unhealthy» lifestyle and metabolic disorders is well established. The important role of dysbiosis of the intestinal microbiota in the NAFLD pathogenesis and the functioning of the intestine‑liver axis is emphasized. Data on the structure and functioning of the intestinal barrier in physiological conditions are presented. It has been proven that the presence of dysbiotic changes in the microbiota plays an important role in the disruption of the barrier function of the gastrointestinal tract, which in turn increases the level of physiological translocation of both bacteria and their toxins and their life products. Part of these harmful products comes to the liver through the portal vein (endotoxinemia). The antigens’ overload contributes to the development and progression of NAFLD (up to liver cirrhosis). The intestinal barrier is emphasized to be dynamic and sensitive to changes occurring in the intestine. The increased intestinal permeability and bacterial overgrowth syndrome (which is a source of increased endotoxemia) is observed in patients with NAFLD more frequently than in healthy subjects. Number of studies have revealed that the degree of intestinal permeability in NAFLD patients correlated with the steatosis severity. The factors that most significantly affect intestinal permeability in patients with NAFLD include microbial environment, bile acids, levels of fecal short‑chain fatty acids (mainly butyrate), the metabolism of the essential aromatic amino acid tryptophan, as well as the nature of nutrition, alcohol intake, medicinal preparations, stress, and level of physical activity, which act either directly or through the induction of intestinal microbiota dysbacteriosis. The increased intestinal permeability and its consequence — bacterial translocation, are noticed to be involved in the development of such complications as spontaneous bacterial peritonitis, hepatorenal syndrome, portal vein thrombosis, hepatic encephalopathy, hepatocellular carcinoma.
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Al-Sadi, Rana, Moustafa Youssef, Manmeet Rawat, Shuhong Guo, Karol Dokladny, Mohammad Haque, Martin D. Watterson, and Thomas Y. Ma. "MMP-9-induced increase in intestinal epithelial tight permeability is mediated by p38 kinase signaling pathway activation of MLCK gene." American Journal of Physiology-Gastrointestinal and Liver Physiology 316, no. 2 (February 1, 2019): G278—G290. http://dx.doi.org/10.1152/ajpgi.00126.2018.
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Matrix metalloproteinase-9 (MMP-9) has been implicated as being an important pathogenic factor in inflammatory bowel disease (IBD). MMP-9 is markedly elevated in intestinal tissue of patients with IBD, and IBD patients have a defective intestinal tight-junction (TJ) barrier manifested by an increase in intestinal permeability. The loss of intestinal epithelial barrier function is an important contributing factor in the development and prolongation of intestinal inflammation; however, the role of MMP-9 in intestinal barrier function remains unclear. The purpose of this study was to investigate the effect of MMP-9 on the intestinal epithelial TJ barrier and to delineate the intracellular mechanisms involved by using in vitro (filter-grown Caco-2 monolayers) and in vivo (mouse small intestine recycling perfusion) systems. MMP-9 caused a time- and dose-dependent increase in Caco-2 TJ permeability. MMP-9 also caused an increase in myosin light-chain kinase (MLCK) gene activity, protein expression, and enzymatic activity. The pharmacological MLCK inhibition and siRNA-induced knockdown of MLCK inhibited the MMP-9-induced increase in Caco-2 TJ permeability. MMP-9 caused a rapid activation of the p38 kinase signaling pathway and inhibition of p38 kinase activity prevented the MMP-9-induced increase in MLCK gene activity and the increase in Caco-2 TJ permeability. MMP-9 also caused an increase in mouse intestinal permeability in vivo, which was accompanied by an increase in MLCK expression. The MMP-9-induced increase in mouse intestinal permeability was inhibited in MLCK-deficient mice. These data show for the first time that the MMP-9-induced increase in intestinal TJ permeability in vitro and in vivo was mediated by the p38 kinase signal transduction pathway upregulation of MLCK gene activity and that therapeutic targeting of these pathways can prevent the MMP-9-induced increase in intestinal TJ permeability. NEW & NOTEWORTHY MMP-9 is highly elevated in patients with IBD. IBD patients have compromised intestinal TJ barrier function manifested by an increase in intestinal permeability and intestinal inflammation. This study shows that MMP-9, at clinically achievable concentrations, causes an increase in intestinal TJ permeability in vitro and in vivo. In addition, a MMP-9-induced increase in intestinal TJ permeability was mediated by an increase in MLCK gene and protein expression via the p38 kinase pathway.
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Chen, Lee-Wei, Ying-Ying Wu, and Ching-Mei Hsu. "Bacteroides fragilis decrease intestinal Enterobacteriacease colonization and reverse metronidazole-induced bacterial translocation (120.22)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 120.22. http://dx.doi.org/10.4049/jimmunol.188.supp.120.22.
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Abstract Bacteroides, one of the major bacterial groups in the intestine, maintain a complex relationship with the host. In this study, the role of B. fragilis in intestinal permeability and immunity were examined in C57BL/6 mice receiving oral treatment of metronidazole for 6 days. Metronidazole treatment significantly decreased the number of B. fragilis but increased that of Enterobacteriaceae in intestinal mucosa and lumen. Metronidazole treatment increased intestinal permeability and pathogenic Klebsiella pneumoniae translocation. However, metronidazole did not change the bacterial killing activity and expression of TLR4, TLR2, MyD88, RegIIIβ, RegIIIγ, CRP-ductin, RELMβ, as well as defensin proteins in intestinal mucosa. Supplementation of dead B. fragilis in drinking water reversed the effects of metronidazole on intestinal permeability, Enterobacteriaceae colonization, and bacterial translocation (BT), suggesting that B. fragilis maintains intestinal permeability and decreases BT through reducing the colonization of Enterobacteriaceae rather than enhancing the expression of antibacterial proteins or the bacterial killing activity. This is further supported by that B. fragilis monoassociated mice showed a decrease of K. pneumoniae translocation and no change in bacterial killing activity as well as expression of defensin and nondefensin protein expression except of CRP-ductin when compared with germ free mice.
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Kubes, P. "Nitric oxide-induced microvascular permeability alterations: a regulatory role for cGMP." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 6 (December 1, 1993): H1909—H1915. http://dx.doi.org/10.1152/ajpheart.1993.265.6.h1909.
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This study evaluated the physiological effects of compounds that alter guanosine 3',5'-cyclic monophosphate (cGMP) on the increase in vascular protein clearance induced by nitric oxide (NO) synthesis inhibition in the feline small intestine. A lymphatic vessel draining the small bowel was cannulated; vascular protein clearance and intestinal blood flow were measured. N omega-nitro-L-arginine methyl ester (L-NAME), the NO inhibitor, was infused (0.5 mumol/min) into the superior mesenteric artery. Vascular protein clearance increased approximately 4.6-fold, whereas blood flow decreased to 50% of control. Elevation of cGMP by 1) cytosolic guanylate cyclase activation with a NO donor (SIN 1) or 2) a cGMP analogue, 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP) completely prevented the rise in microvascular permeability associated with L-NAME. Moreover, these compounds reduced (almost 90%) baseline vascular protein clearance, whereas inhibition of cytosolic guanylate cyclase with methylene blue significantly increased this parameter. Atrial natriuretic factor (ANF) has been reported to increase tissue cGMP levels and microvascular permeability. In this study, ANF did indeed increase intestinal microvascular permeability however this occurred independent of changes in intestinal cGMP levels. These data support a role for cGMP associated with NO-induced microvascular permeability alterations and raise the possibility that ANF has a cGMP-independent effect on microvascular permeability within the intestine.
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Du, Lijun, John J. Kim, Jinhua Shen, and Ning Dai. "Crosstalk between Inflammation and ROCK/MLCK Signaling Pathways in Gastrointestinal Disorders with Intestinal Hyperpermeability." Gastroenterology Research and Practice 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/7374197.
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The barrier function of the intestine is essential for maintaining the normal homeostasis of the gut and mucosal immune system. Abnormalities in intestinal barrier function expressed by increased intestinal permeability have long been observed in various gastrointestinal disorders such as Crohn’s disease (CD), ulcerative colitis (UC), celiac disease, and irritable bowel syndrome (IBS). Imbalance of metabolizing junction proteins and mucosal inflammation contributes to intestinal hyperpermeability. Emerging studies exploringin vitroandin vivomodel system demonstrate that Rho-associated coiled-coil containing protein kinase- (ROCK-) and myosin light chain kinase- (MLCK-) mediated pathways are involved in the regulation of intestinal permeability. With this perspective, we aim to summarize the current state of knowledge regarding the role of inflammation and ROCK-/MLCK-mediated pathways leading to intestinal hyperpermeability in gastrointestinal disorders. In the near future, it may be possible to specifically target these specific pathways to develop novel therapies for gastrointestinal disorders associated with increased gut permeability.
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Hamilton, M. Kristina, Charlotte C. Ronveaux, Bret M. Rust, John W. Newman, Melissa Hawley, Daniela Barile, David A. Mills, and Helen E. Raybould. "Prebiotic milk oligosaccharides prevent development of obese phenotype, impairment of gut permeability, and microbial dysbiosis in high fat-fed mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 312, no. 5 (May 1, 2017): G474—G487. http://dx.doi.org/10.1152/ajpgi.00427.2016.
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Microbial dysbiosis and increased intestinal permeability are targets for prevention or reversal of weight gain in high-fat (HF) diet-induced obesity (DIO). Prebiotic milk oligosaccharides (MO) have been shown to benefit the host intestine but have not been used in DIO. We hypothesized that supplementation with bovine MO would prevent the deleterious effect of HF diet on the gut microbiota and intestinal permeability and attenuate development of the obese phenotype. C57BL/6 mice were fed a control diet, HF (40% fat/kcal), or HF + prebiotic [6%/kg bovine milk oligosaccharides (BMO) or inulin] for 1, 3, or 6 wk. Gut microbiota and intestinal permeability were assessed in the ileum, cecum, and colon. Addition of BMO to the HF diet significantly attenuated weight gain, decreased adiposity, and decreased caloric intake; inulin supplementation also lowered weight gain and adiposity, but this did not reach significance. BMO and inulin completely abolished the HF diet-induced increase in paracellular and transcellular permeability in the small and large intestine. Both BMO and inulin increased abundance of beneficial microbes Bifidobacterium and Lactobacillus in the ileum. However, inulin supplementation altered phylogenetic diversity and decreased species richness. We conclude that addition of BMO to the HF diet completely prevented increases in intestinal permeability and microbial dysbiosis and was partially effective to prevent weight gain in DIO. NEW & NOTEWORTHY This study provides the first report of the effects of prebiotic bovine milk oligosaccharides on the host phenotype of high-fat diet-induced obesity in mice.
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Lee, Hye-Yeon, Shin-Hae Lee, and Kyung-Jin Min. "The Increased Abundance of Commensal Microbes Decreases Drosophila melanogaster Lifespan through an Age-Related Intestinal Barrier Dysfunction." Insects 13, no. 2 (February 21, 2022): 219. http://dx.doi.org/10.3390/insects13020219.
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Background: Commensal microbiota live in their host with a symbiotic relationship that affects the host’s health and physiology. Many studies showed that microbial load and composition were changed by aging and observed that increasing the abundance and changing the composition of commensal microbes had detrimental effects on host lifespan. We hypothesized that dysbiosis of the intestinal microbiota leads to systemic effects in aging flies as a result of the increased intestinal permeability. Methods: We used the fruit fly, Drosophila melanogaster, laboratory strains w1118, as a model system with many advantages for microbe–host studies. Results: The incidence of intestinal dysfunction was increased with age, and intestinal dysfunction increased the permeability of the fly intestine to resident microbes. The lifespan of flies with an intestinal barrier dysfunction was increased by removal of the microbes. Interestingly, some bacteria were also found in the hemolymph of flies with intestinal barrier dysfunction. Conclusion: Our findings suggest the possibility that, as the host ages, there is an increase in intestinal permeability, which leads to an increased intestinal microbial load and a reduction in the host lifespan. Our data therefore indicate a connection between commensal microbes and host lifespan.
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Nagpal, Ravinder, Tiffany M. Newman, Shaohua Wang, Shalini Jain, James F. Lovato, and Hariom Yadav. "Obesity-Linked Gut Microbiome Dysbiosis Associated with Derangements in Gut Permeability and Intestinal Cellular Homeostasis Independent of Diet." Journal of Diabetes Research 2018 (September 3, 2018): 1–9. http://dx.doi.org/10.1155/2018/3462092.
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This study aimed to determine the association between non-high-fat diet-induced obesity- (non-DIO-) associated gut microbiome dysbiosis with gut abnormalities like cellular turnover of intestinal cells, tight junctions, and mucin formation that can impact gut permeability. We used leptin-deficient (Lepob/ob) mice in comparison to C57BL/6J control mice, which are fed on identical diets, and performed comparative and correlative analyses of gut microbiome composition, gut permeability, intestinal structural changes, tight junction-mucin formation, cellular turnover, and stemness genes. We found that obesity impacted cellular turnover of the intestine with increased cell death and cell survival/proliferation gene expression with enhanced stemness, which are associated with increased intestinal permeability, changes in villi/crypt length, and decreased expression of tight junctions and mucus synthesis genes along with dysbiotic gut microbiome signature. Obesity-induced gut microbiome dysbiosis is also associated with abnormal intestinal organoid formation characterized with decreased budding and higher stemness. Results suggest that non-DIO-associated gut microbiome dysbiosis is associated with changes in the intestinal cell death versus cell proliferation homeostasis and functions to control tight junctions and mucous synthesis-regulating gut permeability.
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Shen, Lijuan, Yonghua Zhou, Xiping Wu, Yuewen Sun, Tao Xiao, Yin Gao, and Jingui Wang. "TREM1 Blockade Ameliorates Lipopolysaccharide-Induced Acute Intestinal Dysfunction through Inhibiting Intestinal Apoptosis and Inflammation Response." BioMed Research International 2021 (April 16, 2021): 1–14. http://dx.doi.org/10.1155/2021/6635452.
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Objective. The lipopolysaccharide- (LPS-) induced acute intestinal dysfunction model has been widely applied in recent years. Here, our aim was to investigate the effect of triggering receptor expressed on myeloid cells-1 (TREM1) inhibitor in LPS-induced acute intestinal dysfunction. Methods. Male rats were randomly assigned into normal (saline injection), model (LPS and saline injection), and LP17 (LPS and LP17 (a synthetic TREM1 inhibitor) injection) groups. The levels of intestinal TREM1 expression were evaluated by immunohistochemistry and western blot. Intestinal permeability and apoptosis were separately assessed by the lactulose/mannitol (L/M) ratio and TUNEL assay. The levels of soluble TREM1 (sTREM1), TNF-α, IL-6, and IL-1β were measured in the plasma and intestinal tissues by ELISA. The expression levels of NF-κB, high-mobility group box 1 (HMGB1), and toll-like receptor 4 (TLR-4) were measured with RT-qPCR and western blot. After transfection with si-TREM1 in LPS-induced intestinal epithelium-6 (IEC-6) cells, p-p65 and p-IκBα levels were detected by western blot. Results. LP17-mediated TREM1 inhibition alleviated the intestine tissue damage in rats with LPS-induced acute intestinal dysfunction. LP17 attenuated the LPS-induced increase in sTREM1, TNF-α, IL-6, and IL-1β levels in the plasma and intestinal tissues. Furthermore, intestine permeability and epithelial cell apoptosis were ameliorated by LP17. LP17 attenuated the LPS-induced increase in the expression of TREM1, HMGB1, TLR-4, and NF-κB in the intestine tissues. In vitro, TREM1 knockdown inactivated the NF-κB signaling in LPS-induced IEC-6 cells. Conclusion. LP17 could ameliorate LPS-induced acute intestinal dysfunction, which was associated with inhibition of intestinal apoptosis and inflammation response.
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Parasram, K., D. Bachetti, and P. Karpowicz. "A54 THE CIRCADIAN CLOCK INFLUENCES JAK/STAT SIGNALING AND GUT PERMEABILITY." Journal of the Canadian Association of Gastroenterology 4, Supplement_1 (March 1, 2021): 11–12. http://dx.doi.org/10.1093/jcag/gwab002.052.
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Abstract Background The circadian clock is a 24-hour feedback loop that drives rhythms in behaviours and physiological processes. This molecular timekeeper consists of the transcription factors, Clock-Cycle, that drive expression of thousands of clock-controlled genes, with two of these, Period and Timeless, acting as negative regulators of Clock-Cycle. This fundamental mechanism was initially characterized in the fruit fly, Drosophila melanogaster (Nobel Prize in Physiology & Medicine, 2017), and is highly conserved in humans. The intestine, or midgut, of Drosophila, is also similar to the human small intestine consisting of similar cellular lineage, signaling pathways, and physiological functions. The lineage of the Drosophila intestine contains the same four cell types as humans: intestinal stem cells (ISCs), progenitors called enteroblasts, enterocytes and enteroendocrine cells. This simplified lineage as well as the genetic tools available, make Drosophila an ideal model for intestinal regeneration in health and disease. We have previously shown that the circadian clock is active in ISCs, EBs and ECs during both homeostatic and regenerating conditions. Furthermore, the circadian clock regulates the mitosis of ISCs under regenerating conditions. Aims We sought to uncover if Jak/STAT signaling, one of the key pathways involved in ISC proliferation in the Drosophila intestine, shows a circadian rhythm and if there is a time-of-day difference in the regenerative response. Methods To test whether the clock regulates Jak/STAT during acute injury, we developed an irradiation assay that does not affect survival but acutely disrupts intestinal barrier function. Results Using a dynamic reporter of Jak/STAT activity we show that Period circadian clock mutants have low Jak/STAT signaling and a leaky gut phenotype. Wildtype controls show time-dependent gut leakiness upon irradiation, which is higher and time-independent in Period mutants. The level of Jak/STAT response differs depending on the time of irradiation in the controls, but is higher at all times in the mutants. Conclusions The Jak/Stat pathway regulates intestinal immunity and epithelial cell proliferation in humans, thus playing a role in colorectal cancer and inflammatory bowel disease. Our results suggest Jak/Stat is controlled by the circadian clock, which has implications for intestinal recovery following medical treatments, including radiation therapy. Funding Agencies NRC
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Di Tommaso, Natalia, Francesco Santopaolo, Antonio Gasbarrini, and Francesca Romana Ponziani. "The Gut–Vascular Barrier as a New Protagonist in Intestinal and Extraintestinal Diseases." International Journal of Molecular Sciences 24, no. 2 (January 12, 2023): 1470. http://dx.doi.org/10.3390/ijms24021470.
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The intestinal barrier, with its multiple layers, is the first line of defense between the outside world and the intestine. Its disruption, resulting in increased intestinal permeability, is a recognized pathogenic factor of intestinal and extra-intestinal diseases. The identification of a gut–vascular barrier (GVB), consisting of a structured endothelium below the epithelial layer, has led to new evidence on the etiology and management of diseases of the gut–liver axis and the gut–brain axis, with recent implications in oncology as well. The gut–brain axis is involved in several neuroinflammatory processes. In particular, the recent description of a choroid plexus vascular barrier regulating brain permeability under conditions of gut inflammation identifies the endothelium as a key regulator in maintaining tissue homeostasis and health.
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Novosad, Veronica L., Jennifer L. Richards, Neil A. Phillips, Michelle A. King, and Thomas L. Clanton. "Regional susceptibility to stress-induced intestinal injury in the mouse." American Journal of Physiology-Gastrointestinal and Liver Physiology 305, no. 6 (September 15, 2013): G418—G426. http://dx.doi.org/10.1152/ajpgi.00166.2013.
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Injury to the intestinal mucosa is a life-threatening problem in a variety of clinical disorders, including hemorrhagic shock, trauma, burn, pancreatitis, and heat stroke. The susceptibility to injury of different regions of intestine in these disorders is not well understood. We compared histological injury across the small intestine in two in vivo mouse models of injury, hemorrhagic shock (30% loss of blood volume) and heat stroke (peak core temperature 42.4°C). In both injury models, areas near the duodenum showed significantly greater mucosal injury and reductions in villus height. To determine if these effects were dependent on circulating factors, experiments were performed on isolated intestinal segments to test for permeability to 4-kDa FITC-dextran. The segments were exposed to hyperthermia (42°C for 90 min), moderate simulated ischemia (Po2 ∼30 Torr, Pco2 ∼60 Torr, pH 7.1), severe ischemia (Po2 ∼20 Torr, Pco2 ∼80 Torr, pH 6.9), or severe hypoxia (Po2 ∼0 Torr, Pco2 ∼35 Torr) for 90 min, and each group was compared with sham controls. All treatments resulted in marked elevations in permeability within segments near the duodenum. In severe hypoxia or hyperthermia, permeability was also moderately elevated in the jejunum and ileum; in moderate or severe ischemia, permeability was unaffected in these regions. The results demonstrate increased susceptibility of proximal regions of the small intestine to acute stress-induced damage, irrespective of circulating factors. The predominant injury in the duodenum may impact the pattern of acute inflammatory responses arising from breach of the intestinal barrier, and such knowledge may be useful for designing therapeutic strategies.
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Hardin, J. A., L. Donegan, R. C. Woodman, C. Trevenen, and D. G. Gall. "Mucosal inflammation in a genetic model of spontaneous type I diabetes mellitus." Canadian Journal of Physiology and Pharmacology 80, no. 11 (November 1, 2002): 1064–70. http://dx.doi.org/10.1139/y02-138.
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The BioBreeding (BB) rat provides a model of spontaneous type I diabetes mellitus that closely resembles the human disease. Diabetes-prone BB rats demonstrate increased intestinal permeability prior to the development of insulinitis. Studies suggest that alterations in intestinal permeability can lead to increased intestinal inflammatory activity. Diabetes-prone (BBdp) and diabetes-resistant (BBdr) BB rats were examined at 45 days and at >70 days of age following the development of clinical disease (BBd). In separate experiments, tissue was assayed for myeloperoxidase (MPO) or fixed for histological assessment and immunohistochemistry. Blood was obtained for leukocyte MPO measurements and morphological assessment of circulating leukocytes. MPO activity was significantly elevated in the distal small intestine of 45-day-old BBdp rats. In contrast, at >70 days of age, MPO activity was significantly increased throughout the small intestine of BBd and non-diabetic BBdp rats. Subsequently, all measurements were performed in >70-day-old rats. An increase in inflammatory infiltrate was noted in the distal small intestine of BBd rats by light microscopy. Infiltrating cells were identified as bands (a maturing cell type of the neutrophil lineage) and mature neutrophils. The findings suggest diabetes susceptibility is associated with an increase in intestinal inflammatory activity.Key words: diabetes, inflammation, myeloperoxidase, jejunum.
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Lifschitz, Carlos. "Intestinal Permeability." Journal of Pediatric Gastroenterology and Nutrition 4, no. 4 (August 1985): 520–22. http://dx.doi.org/10.1097/00005176-198508000-00003.
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Bjarnason, I. "Intestinal permeability." Gut 35, no. 1 Suppl (January 1, 1994): S18—S22. http://dx.doi.org/10.1136/gut.35.1_suppl.s18.
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Gardiner, K. R., R. J. Maxwell, B. J. Rowlands, and G. R. Barclay. "Intestinal permeability." Gut 37, no. 4 (October 1, 1995): 589. http://dx.doi.org/10.1136/gut.37.4.589.
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Struthers, G. R., D. J. Andrews, R. J. C. Gilson, G. A. Reynolds, T. Low-Beer, Norman Veall, A. J. Williams, and S. E. Church. "INTESTINAL PERMEABILITY." Lancet 325, no. 8428 (March 1985): 587–88. http://dx.doi.org/10.1016/s0140-6736(85)91251-6.
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Cobden, I. "Intestinal permeability." Gut 29, no. 5 (May 1, 1988): 693. http://dx.doi.org/10.1136/gut.29.5.693.
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Perdue, M. "Intestinal permeability." Gut 29, no. 7 (July 1, 1988): 1016. http://dx.doi.org/10.1136/gut.29.7.1016.
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Xu, Mengyi, Kangkang Luo, Junjie Li, Yu Li, Yuxuan Zhang, Zhiyao Yuan, Qiang Xu, and Xudong Wu. "Role of Intestinal Microbes in Chronic Liver Diseases." International Journal of Molecular Sciences 23, no. 20 (October 21, 2022): 12661. http://dx.doi.org/10.3390/ijms232012661.
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With the recent availability and upgrading of many emerging intestinal microbes sequencing technologies, our research on intestinal microbes is changing rapidly. A variety of investigations have found that intestinal microbes are essential for immune system regulation and energy metabolism homeostasis, which impacts many critical organs. The liver is the first organ to be traversed by the intestinal portal vein, and there is a strong bidirectional link between the liver and intestine. Many intestinal factors, such as intestinal microbes, bacterial composition, and intestinal bacterial metabolites, are deeply involved in liver homeostasis. Intestinal microbial dysbiosis and increased intestinal permeability are associated with the pathogenesis of many chronic liver diseases, such as alcoholic fatty liver disease (AFLD), non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), chronic hepatitis B (CHB), chronic hepatitis C (CHC), autoimmune liver disease (AIH) and the development of hepatocellular carcinoma (HCC). Intestinal permeability and dysbacteriosis often lead to Lipopolysaccharide (LPS) and metabolites entering in serum. Then, Toll-like receptors activation in the liver induces the exposure of the intestine and liver to many small molecules with pro-inflammatory properties. And all of these eventually result in various liver diseases. In this paper, we have discussed the current evidence on the role of various intestinal microbes in different chronic liver diseases. As well as potential new therapeutic approaches are proposed in this review, such as antibiotics, probiotics, and prebiotics, which may have an improvement in liver diseases.
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Lanza, Marika, Alessia Filippone, Giovanna Casili, Letterio Giuffrè, Sarah Adriana Scuderi, Irene Paterniti, Michela Campolo, Salvatore Cuzzocrea, and Emanuela Esposito. "Supplementation with SCFAs Re-Establishes Microbiota Composition and Attenuates Hyperalgesia and Pain in a Mouse Model of NTG-Induced Migraine." International Journal of Molecular Sciences 23, no. 9 (April 27, 2022): 4847. http://dx.doi.org/10.3390/ijms23094847.
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Migraine is a common brain-disorder that affects 15% of the population. Converging evidence shows that migraine is associated with gastrointestinal disorders. However, the mechanisms underlying the interaction between the gut and brain in patients with migraine are not clear. In this study, we evaluated the role of the short-chain fatty acids (SCFAs) as sodium propionate (SP) and sodium butyrate (SB) on microbiota profile and intestinal permeability in a mouse model of migraine induced by nitroglycerine (NTG). The mice were orally administered SB and SP at the dose of 10, 30 and 100 mg/kg, 5 min after NTG intraperitoneal injections. Behavioral tests were used to evaluate migraine-like pain. Histological and molecular analyses were performed on the intestine. The composition of the intestinal microbiota was extracted from frozen fecal samples and sequenced with an Illumina MiSeq System. Our results demonstrated that the SP and SB treatments attenuated hyperalgesia and pain following NTG injection. Moreover, SP and SB reduced histological damage in the intestine and restored intestinal permeability and the intestinal microbiota profile. These results provide corroborating evidence that SB and SP exert a protective effect on central sensitization induced by NTG through a modulation of intestinal microbiota, suggesting the potential application of SCFAs as novel supportive therapies for intestinal disfunction associated with migraine.
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Dublineau, I., F. Lebrun, S. Grison, and N. M. Griffiths. "Functional and structural alterations of epithelial barrier properties of rat ileum following X-irradiation." Canadian Journal of Physiology and Pharmacology 82, no. 2 (February 1, 2004): 84–93. http://dx.doi.org/10.1139/y03-129.
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Irradiation of the digestive system leads to alterations of the small intestine. We have characterized the disruption of the barrier integrity in rat ileum from 1 to 14 days following irradiation ranging from 6 to 12 Gy. The intestinal permeability to 14C-mannitol and 3H-dextran 70 000 was measured in vitro in Ussing chambers. In parallel to these functional studies, immunohistochemical analyses of junctional proteins (ZO-1 and β-catenin) of ileal epithelium were performed by confocal microscopy. Irradiation with 10 Gy induced a marked decrease in epithelial tissue resistance at three days and a fivefold increase in mannitol permeability, without modifications of dextran permeability. A disorganization of the localization for ZO-1 and β-catenin was also observed. At 7 days after irradiation, we observed a recovery of the organization of junctional proteins in parallel to a return of intestinal permeability to control value. In addition to these time-dependent effects, a gradual effect on epithelial integrity of the radiation doses was observed 3 days after irradiation. This study shows a disruption of the integrity of the intestinal barrier in rat ileum following abdominal X-irradiation, depending on the time postirradiation and on the delivered dose. The loss of barrier integrity was characterized by a disorganization of proteins of tight and adherent junctions, leading to increased intestinal permeability to mannitol.Key words: intestinal permeability, ZO-1, β-catenin, tight and adherent junctions.
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MohanKumar, Krishnan, Kopperuncholan Namachivayam, Nithya Sivakumar, Natascha G. Alves, Venkataramana Sidhaye, Jayanta K. Das, Yerin Chung, Jerome W. Breslin, and Akhil Maheshwari. "Severe neonatal anemia increases intestinal permeability by disrupting epithelial adherens junctions." American Journal of Physiology-Gastrointestinal and Liver Physiology 318, no. 4 (April 1, 2020): G705—G716. http://dx.doi.org/10.1152/ajpgi.00324.2019.
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Anemia is a frequent diagnosis in critically ill infants, but the clinical implications of severe anemia in these patients remain unclear. In this study, we examined preweaned mice to investigate the effects of severe anemia during early infancy on gut mucosal permeability. C57BL/6 mice were subjected to timed phlebotomy between postnatal days (P) 2–10 to induce severe anemia (hematocrits 20%–24%), and intestinal permeability was tracked longitudinally between P10 and P20 as intestine-to-plasma translocation of enteral macromolecules and bacterial translocation. Epithelial junctions were evaluated by electron microscopy, polymerase chain reactions, immunohistochemistry, and/or enzyme immunoassays on intestinal tissues, Caco-2 intestinal epithelial-like cells, and colonic organoids. Preweaned mouse pups showed an age-related susceptibility to severe anemia, with increased intestinal permeability to enteral macromolecules (dextran, ovalbumin, β-lactoglobulin) and luminal bacteria. Electron micrographs showed increased paracellular permeability and ultrastructural abnormalities of the adherens junctions. These findings were explained by the loss of E-cadherin in epithelial cells, which was caused by destabilization of the E-cadherin ( Cdh1) mRNA because of microRNA let-7e-5p binding to the 3′-untranslated region. Severe anemia resulted in a disproportionate and persistent increase in intestinal permeability in preweaned mice because of the disruption of epithelial adherens junctions. These changes are mediated via microRNA let-7e-mediated depletion of Cdh1 mRNA. NEW & NOTEWORTHY This research article shows that newborn infants with severe anemia show an age-related susceptibility to developing increased intestinal permeability to ingested macromolecules. This abnormal permeability develops because of abnormalities in intestinal epithelial junctions caused by a deficiency of the molecule E-cadherin in epithelial cells. The deficiency of E-cadherin is caused by destabilization of its mRNA precursor because of increased expression and binding of another molecule, the microRNA let-7e-5p, to the E-cadherin mRNA.
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Knudsen, David, Fredrik Jutfelt, Henrik Sundh, Kristina Sundell, Wolfgang Koppe, and Hanne Frøkiær. "Dietary soya saponins increase gut permeability and play a key role in the onset of soyabean-induced enteritis in Atlantic salmon (Salmo salar L.)." British Journal of Nutrition 100, no. 1 (July 2008): 120–29. http://dx.doi.org/10.1017/s0007114507886338.
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Saponins are naturally occurring amphiphilic molecules and have been associated with many biological activities. The aim of the present study was to investigate whether soya saponins trigger the onset of soyabean-induced enteritis in Atlantic salmon (Salmo salar L.), and to examine if dietary soya saponins increase the epithelial permeability of the distal intestine in Atlantic salmon. Seven experimental diets containing different levels of soya saponins were fed to seawater-adapted Atlantic salmon for 53 d. The diets included a fishmeal-based control diet, two fishmeal-based diets with different levels of added soya saponins, one diet containing 25 % lupin kernel meal, two diets based on 25 % lupin kernel meal with different levels of added soya saponins, and one diet containing 25 % defatted soyabean meal. The effect on intestinal morphology, intestinal epithelial permeability and faecal DM content was examined. Fish fed 25 % defatted soyabean meal displayed severe enteritis, whereas fish fed 25 % lupin kernel meal had normal intestinal morphology. The combination of soya saponins and fishmeal did not induce morphological changes but fish fed soya saponins in combination with lupin kernel meal displayed significant enteritis. Increased epithelial permeability was observed in fish fed 25 % defatted soyabean meal and in fish fed soya saponin concentrate independent of the protein source in the feed. The study demonstrates that soya saponins, in combination with one or several unidentified components present in legumes, induce an inflammatory reaction in the distal intestine of Atlantic salmon. Soya saponins increase the intestinal epithelial permeability but do not, per se, induce enteritis.
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El Wakeel, Maged A., Ghada M. El-Kassas, Gihan Fouad Ahmed, Walaa H. Ali, Eman Mohamed Elsheikh, Salwa Refat El-Zayat, Nevein N. Fadl, Eman H. Kamel, and Thanaa M. Rabah. "Fecal Markers of Environmental Enteric Dysfunction and their Relation to Faltering Growth in a Sample of Egyptian Children." Open Access Macedonian Journal of Medical Sciences 9, B (October 10, 2021): 1117–22. http://dx.doi.org/10.3889/oamjms.2021.7029.
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BACKGROUND: Chronic malnutrition is a long-term health condition that has threatening effects on children’s health. Environmental enteric dysfunction (EED) is a subclinical disorder affecting the small intestine that may occur due to exposure to environmental pathogens and toxins. AIM: The present research was intended to detect the value of fecal biomarkers of intestinal epithelial damage alpha-1anti-trypsin (AAT) and intestinal inflammation Myeloperoxidase (MPO) and Neopetrin (NEO), also to quantify their association with faltering growth in stunted and underweight children. PATIENTS AND METHODS: This case–control study included 105 children with moderate malnutrition as a case group and 100 children of normal body weight and height as a control group. Quantification of fecal markers levels of intestinal permeability AAT and intestinal inflammation (NEO and MPO) along with serum micronutrients levels (iron and zinc) in children with malnutrition in comparison to controls. RESULTS: Fecal markers of intestinal permeability AAT and intestinal inflammation NEO had statistically significant higher levels in children with malnutrition, while serum micronutrients (iron and zinc) had statistically significant lower levels in children with malnutrition. CONCLUSION: Faltering growth is associated with elevated fecal markers of intestinal permeability AAT and intestinal inflammation NEO. EED may be a cause for faltering growth.
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Liu, Xin, Pei Wu, Wei-Dan Jiang, Yang Liu, Jun Jiang, Sheng-Yao Kuang, Ling Tang, Xiao-Qiu Zhou, and Lin Feng. "Effects of Dietary Ochratoxin A on Growth Performance and Intestinal Apical Junctional Complex of Juvenile Grass Carp (Ctenopharyngodon idella)." Toxins 13, no. 1 (December 24, 2020): 11. http://dx.doi.org/10.3390/toxins13010011.
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Ochratoxin A (OTA) contamination widely occurs in various feed ingredients and food crops, potentially posing a serious health threat to animals. In this research, 1260 juvenile grass carp were separately fed with seven distinct experimental diets (0, 406, 795, 1209, 1612, 2003 and 2406 µg of OTA/kg of diet) for 60 consecutive days to evaluate OTA’s toxic effect on the intestinal apical junctional complex (including the tight junction (TJ) and the adherents junction (AJ)) and the underlying action mechanisms. Our experiment firstly confirmed that OTA caused fish growth retardation and disrupted the intestinal structural integrity. The detailed results show that OTA (1) depressed the feed efficiency, percentage weight gain and specific growth rate; (2) accumulated in the intestine; (3) caused oxidative damage and increased intestinal permeability; and (4) induced the RhoA/ROCK signaling pathway, destroying intestinal apical junctional complexes. Notably, OTA intervention did not result in changes in the gene expression of claudin-3c (in the proximal intestine (PI)), claudin-b and ZO-2b (in the mid intestine (MI) and distal intestine (DI)) in the fish intestine.
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Savarina, V. A., and V. M. Mitsura. "THE ROLE OF THE GUT-LIVER AXIS IN LIVER CIRRHOSIS PATHOGENESIS AND COMPLICATIONS." Hepatology and Gastroenterology 4, no. 2 (2020): 151–54. http://dx.doi.org/10.25298/2616-5546-2020-4-2-151-154.
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Background. Liver cirrhosis is a severe disease that can provoke hepatocellular carcinoma. It is known that such patients have increased intestinal permeability causing the translocation of living bacteria and bacterial products through the inferior vena cava system into the liver, that leads to a cascade of immune and molecular events. Objective – to establish the role of the gut-liver axis in the pathogenesis and outcomes of liver cirrhosis. Material and methods. We performed a PubMed search of publications over the last 10 years, using the keywords ‘intestinal permeability’, ‘cirrhosis’. Results. Increased intestinal permeability and bacterial translocation are of great importance in the development of liver cirrhosis. In turn, the progression of the disease further enhances the transfer of bacteria from the intestine into the inferior vena cava system. The severity of this process is proportional to the stage of cirrhosis and correlates with the prognosis of the disease. Conclusion. Increased intestinal permeability, altered gut microbiota and bacterial translocation contribute to liver damage and fbrosis up to the development of liver cirrhosis and its complications. Further research is required to determine if modulation of the gut microbiota can affect the course of liver disease.