Relevant bibliographies by topics / Epithelial permeability

Academic literature on the topic 'Epithelial permeability'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Epithelial permeability"

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Maharshak, Nitsan, Eun Young Huh, Chorlada Paiboonrungruang, Michael Shanahan, Lance Thurlow, Jeremy Herzog, Zorka Djukic, et al. "Enterococcus faecalis Gelatinase Mediates Intestinal Permeability via Protease-Activated Receptor 2." Infection and Immunity 83, no. 7 (April 27, 2015): 2762–70. http://dx.doi.org/10.1128/iai.00425-15.

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Microbial protease-mediated disruption of the intestinal epithelium is a potential mechanism whereby a dysbiotic enteric microbiota can lead to disease. This mechanism was investigated using the colitogenic, protease-secreting enteric microbeEnterococcus faecalis. Caco-2 and T-84 epithelial cell monolayers and the mouse colonic epithelium were exposed to concentrated conditioned media (CCM) fromE. faecalisV583 andE. faecalislacking the gelatinase gene (gelE). The flux of fluorescein isothiocyanate (FITC)-labeled dextran across monolayers or the mouse epithelium following exposure to CCM from parental or mutantE. faecalisstrains indicated paracellular permeability. A protease-activated receptor 2 (PAR2) antagonist and PAR2-deficient (PAR2−/−) mice were used to investigate the role of this receptor inE. faecalis-induced permeability. Gelatinase (GelE) purified fromE. faecalisV583 was used to confirm the ability of this protease to induce epithelial cell permeability and activate PAR2. The protease-mediated permeability of colonic epithelia from wild-type (WT) and PAR2−/−mice by fecal supernatants from ulcerative colitis patients was assessed. SecretedE. faecalisproteins induced permeability in epithelial cell monolayers, which was reduced in the absence ofgelEor by blocking PAR2 activity. SecretedE. faecalisproteins induced permeability in the colonic epithelia of WT mice that was absent in tissues from PAR2−/−mice. Purified GelE confirmed the ability of this protease to induce epithelial cell permeability via PAR2 activation. Fecal supernatants from ulcerative colitis patients induced permeability in the colonic epithelia of WT mice that was reduced in tissues from PAR2−/−mice. Our investigations demonstrate that GelE fromE. faecaliscan regulate enteric epithelial permeability via PAR2.
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Lewis, S. A., J. R. Berg, and T. J. Kleine. "Modulation of epithelial permeability by extracellular macromolecules." Physiological Reviews 75, no. 3 (July 1, 1995): 561–89. http://dx.doi.org/10.1152/physrev.1995.75.3.561.

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Epithelia are sheets of cells joined together by tight junctions. This geometry allows an epithelium to act as a barrier, i.e., restrict the movement of substances between two compartments that it separates (typically 1 compartment is the blood) and also to actively and selectively transport substances between the two compartments. It has been known for a number of years that both the barrier and transport functions of epithelia can be regulated by hormones and neurotransmitters, and this regulation is a central component of plasma electrolyte and nonelectrolyte homeostasis. Less appreciated is that these epithelial functions can be modified by macromolecules other than neurotransmitters and hormones. These macromolecules have been divided into the following categories: proteases, cytokines, cellular constituents, nonbacterial xenobiotics, and bacterial xenobiotics. Such macromolecules can alter epithelial transport and barrier function by a number of different mechanisms. These include proteolysis of epithelial ion channels and tight junctional complexes, conversion of an ion pump into a nonselective cation channel, increase in epithelial membrane permeability resulting in cell swelling and lysis, and up- or downregulation of cellular second messenger systems that can alter ion transport capabilities or prove cytotoxic to the cells. Finally, these modifications can be either transient or chronic in nature and in many circumstances result in a perturbation of the electrolyte and nonelectrolyte status of the host organism.
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Negrete, H. O., J. P. Lavelle, J. Berg, S. A. Lewis, and M. L. Zeidel. "Permeability properties of the intact mammalian bladder epithelium." American Journal of Physiology-Renal Physiology 271, no. 4 (October 1, 1996): F886—F894. http://dx.doi.org/10.1152/ajprenal.1996.271.4.f886.

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Because the mammalian bladder must store urine of composition which differs markedly from that of plasma for prolonged periods, the bladder permeability barrier must maintain extremely low permeabilities to substances which normally cross membranes relatively rapidly, such as water, protons, and small nonelectrolytes like urea and ammonia. In the present studies, permeabilities of the apical membrane of dissected rabbit bladder epithelium to water, urea, ammonia, and protons were measured in Ussing chambers and averaged (in cm/s) for water, 5.15 +/- 0.43 x 10(-5); for urea, 4.51 +/- 0.67 x 10(-6); for ammonia, 5.14 +/- 0.62 x 10(-4); and for protons, 2.98 +/- 1.87 x 10(-3), respectively. These permeability values are exceptionally low and are expected to result in minimal to no leakage of these normally permeable substances across the epithelium. Water permeabilities in intact whole rabbit bladders were indistinguishable from those obtained in the dissected epithelial preparation. Moreover, addition of nystatin to the apical solution of dissected epithelia rapidly increased water permeability in conjunction with loss of epithelial resistance. These results confirm that the apical membrane of the bladder epithelial cells represents the bladder permeability barrier. In addition, they establish a model system that will permit examination of how membrane structure reduces permeability and how epithelial injury compromises barrier function.
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Ludwigs, Ulf, Anders Philip, Bengt Robertson, and Göran Hedenstierna. "Pulmonary Epithelial Permeability." Chest 110, no. 2 (August 1996): 486–93. http://dx.doi.org/10.1378/chest.110.2.486.

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LANGFORD, J. A., C. A. LEWIS, A. R. GELLERT, S. E. J. TOLFREE, and R. M. RUDD. "Pulmonary epithelial permeability." Nuclear Medicine Communications 7, no. 3 (March 1986): 183–90. http://dx.doi.org/10.1097/00006231-198603000-00006.

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Peterson, Michael W., and Jennifer Kirschbaum. "Asbestos-induced lung epithelial permeability: potential role of nonoxidant pathways." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 2 (August 1, 1998): L262—L268. http://dx.doi.org/10.1152/ajplung.1998.275.2.l262.

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Asbestos fibers are an important cause of lung fibrosis; however, the biological mechanisms are incompletely understood. The lung epithelium serves an important barrier function in the lung, and disrupting the epithelial barrier can contribute to lung fibrosis. Lung epithelial permeability is increased in patients with asbestosis, and asbestos fibers increase permeability across cultured human lung epithelium. However, the mechanism of this increased permeability is not known. Many of the biological effects of asbestos are postulated to be due to its ability to generate oxidants, and oxidants are known to increase epithelial permeability. However, we previously reported that altering the iron content of asbestos (important in oxidant generation) had no effect on its ability to increase permeability. For that reason, we undertook these studies to determine whether asbestos increases epithelial permeability through nonoxidant pathways. Both extracellular (H2O2) and intracellular (menadione) oxidants increase paracellular permeability across human lung epithelial monolayers. Extracellular catalase but not superoxide dismutase prevented increased permeability after both oxidant exposures. However, catalase offered no protection from asbestos-induced permeability. We next depleted the cells of glutathione or catalase to determine whether depleting normal cellular antioxidants would increase the sensitivity to asbestos. Permeability was the same in control cells and in cells depleted of these antioxidants. In addition to generating oxidants, asbestos also activates signal transduction pathways. Blocking protein kinase C activation did not prevent asbestos-induced permeability; however, blocking tyrosine kinase with tyrophostin A25 did prevent asbestos-induced permeability, and blocking tyrosine phosphatase with sodium vanadate enhanced the effect of asbestos. These data demonstrate that asbestos may increase epithelial permeability through nonoxidant pathways that involve tyrosine kinase activation. This model offers an important system for studying pathways involved in regulating lung epithelial permeability.
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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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Merchant, R. K., M. W. Peterson, and G. W. Hunninghake. "Silica directly increases permeability of alveolar epithelial cells." Journal of Applied Physiology 68, no. 4 (April 1, 1990): 1354–59. http://dx.doi.org/10.1152/jappl.1990.68.4.1354.

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Alveolar epithelial cell injury and increased alveolar-capillary membrane permeability are important features of acute silicosis. To determine whether silica particles contribute directly to this increased permeability, we measured paracellular permeability of rat alveolar epithelium after exposure to silica, in vitro, using markers of the extracellular space. Silica (Minusil) markedly increased permeability in a dose- and time-dependent manner. This was not the result of cytolytic injury, because lactate dehydrogenase release from monolayers exposed to silica was not increased. Pretreatment of the silica with serum, charged dextrans, or aluminum sulfate blocked the increase in permeability. Scanning electron microscopy demonstrated adherence of the silica to the surface of the alveolar epithelial cells. Thus silica can directly increase permeability of alveolar epithelium.
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Moseley, P. L., C. Gapen, E. S. Wallen, M. E. Walter, and M. W. Peterson. "Thermal stress induces epithelial permeability." American Journal of Physiology-Cell Physiology 267, no. 2 (August 1, 1994): C425—C434. http://dx.doi.org/10.1152/ajpcell.1994.267.2.c425.

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The mechanisms by which heat injury results in multiorgan system failure are unknown, but the presence of endotoxemia and intestinal hemorrhage suggests that changes in gut epithelial permeability may be crucial to this process. To determine whether alterations in epithelial permeability occur at physiologically relevant temperatures, heat-induced changes on epithelial barrier integrity were studied using a high-resistance clone of Madin-Darby canine kidney epithelial cells. Transepithelial electrical conductance increased when monolayers were heated above 38.3 degrees C. Early changes in conductance were completely reversible with cooling. Increased conductance was due to increased paracellular permeability because heat also induced increased mannitol permeability across the monolayers. A conditioning heat stress (42 degrees C for 90 min) altered heat-induced permeability. When cell monolayers were exposed to this conditioning stress 48 h before measurement of conductance with increasing temperatures, the conductance increase did not occur until they were heated to 39.4 degrees C compared with 38.8 degrees C in naive control cells. This conditioning treatment also conferred thermotolerance as measured by cell survival after a lethal 45.0 degrees C heat stress. There was no difference in the temperature at which conductance increased between preheated and control cells 96 h after a preconditioning heat stress. The conditioning heat stress resulted in accumulation of heat-shock protein (HSP) 70 in cells at 48 h, but HSP 70 returned to control levels at 96 h. These studies demonstrate that small temperature elevations increase epithelial permeability and that prior heat stress which induces HSP 70 shifts the threshold temperature required to disrupt the epithelium.
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Min, Hyun Jin, Tae Hoon Kim, Joo-Heon Yoon, and Chang-Hoon Kim. "Hypoxia Increases Epithelial Permeability in Human Nasal Epithelia." Yonsei Medical Journal 56, no. 3 (2015): 825. http://dx.doi.org/10.3349/ymj.2015.56.3.825.

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Dissertations / Theses on the topic "Epithelial permeability"

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Dennison, Patrick Winford. "Epithelial permeability in asthma." Thesis, University of Southampton, 2017. https://eprints.soton.ac.uk/416625/.

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Our knowledge and understanding of asthma have evolved over time, leading to new and improved treatments for this disease. Despite existing treatments however, there remains to date a significant proportion of asthmatics who remain poorly controlled, with unmet needs. Most existing treatments are based on the Th2-driven inflammation model of asthma, however there is increasing recognition of the importance of the epithelium in asthma pathogenesis. It has been proposed that the asthmatic epithelium is chronically damaged and unable to repair, with increased permeability as a result. Existing treatments do not address the epithelial damage directly, however there are now available recombinant growth factors that have been shown to have beneficial effects on epithelial healing. Our hypothesis was that modification of the epithelium, in effect boosting its repair using recombinant human keratinocyte growth factor (rhKGF), would lead to improvement in clinical parameters. This was explored in several fashions. Firstly a randomised, double-blind, placebo-controlled clinical trial was performed using 20 poorly controlled, moderate asthmatics, with the active treatment group receiving parenteral rhKGF. Assessments before and after drug administration included objective, clinically relevant, measures of asthma such as airway hyperresponsiveness (AHR) measurements, spirometric measures, exhaled nitric oxide measurements and peak flow recording. Subjective, patient-centred assessments were also made using questionnaires to assess asthma control and quality of life, and bronchoscopy was performed to obtain samples to measure biological effects of the drug. KGF treatment resulted in a significantly greater improvement in the primary outcome of mannitol AHR, together with greater improvements in quality of life in the active treatment group compared to placebo. Other features (such as methacholine AHR, asthma control questionnaire scores, spirometric values, exhaled nitric oxide and peak flow variability) did not differ significantly between the groups, although this may be due to a greater than expected placebo response. Biological outcomes also did not differ significantly between the groups, although this may have been due to the sampling time-point used. Concurrently to the clinical trial above, in vitro experiments were performed on cell cultures of epithelial cells from asthmatic and healthy donors, to verify and further explore the effects of KGF on an asthmatic epithelium. Specifically mechanical wounds were inflicted on the cultures, with assessment of the repair process using wound imaging, measurement of trans-epithelial electrical resistance (TER) and permeability to FITC-labelled dextran, in the presence and absence of KGF. As a subset of these experiments, some cultures were exposed to mechanical compression using air pressure, as a mimic for bronchoconstriction, to see if KGF was effective in these circumstances. Results confirm a biological effect for KGF on wound repair in the asthmatic epithelium, which can also partially overcome the deleterious effect of compression on wound healing. An intrinsic difference in wound healing between asthmatic and healthy cohorts, as previously reported, was not apparent. Lastly the potential of nuclear medicine imaging, to assess epithelial permeability, was explored, for its potential use in future studies of asthma treatments addressing the epithelium directly. Unfortunately this was halted after a pilot study suggested potential methodological flaws – the results and conclusions from this pilot study are presented here, with suggestions for future studies in this area.
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Anderson, Keith G. "Modulation and quantitation of epithelial paracellular permeability." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324937.

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Collares, Buzato Carla Beatriz. "Modulation of paracellular permeability and intercellular junctions in cultured epithelia." Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283019.

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Shang, Valerie C. M. "The effects of endocannabinoids and phytocannabinoids on bronchial epithelial permeability." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/31264/.

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Injury to the bronchial epithelium in respiratory diseases such as asthma and COPD results in the loss of barrier function and an elevated sensitivity to environmental insults. An increased release of the endogenous cannabinoid, anandamide in response to inhalation of allergen in asthmatic patients has been reported. In contrast, previous clinical trial findings suggest anti-inflammatory and broncho-relaxant properties of the phytocannabinoid, ∆9-tetrahydrocannabinol (THC). The aim of this study was, therefore, to determine the effects of endocannabinoids and phytocannabinoids on bronchial epithelial cell permeability and to investigate the mechanisms involved. Calu-3 human bronchial epithelial cells were cultured at air-liquid interface to allow development of tight junctions. Changes in transepithelial electrical resistance (TEER), a reflection of epithelial permeability, were measured at various time points post-treatment. The endogenous cannabinoid anandamide produced a significant reduction in TEER, which was unaffected by cannabinoid receptor antagonists, but attenuated by URB597, an inhibitor of fatty acid amide hydrolase, and by a combination of cyclooxygenase and lipooxygenase blockade. Subsequent immunoblotting data revealed that the expression of tight junction proteins, occludin and ZO-1, were also reduced by anandamide. Inhibition of ERK activation by MEK1/2 inhibitors, PD98059 and U0126, prevented the anandamide-induced reduction in TEER and prevented the reduction in occludin expression. Thus, ERK activation is likely to mediate these effects by altering the expression of tight junction proteins. Treatment with THC prevented TNFα-induced decrease in TEER and increased in paracellular permeability. CB1 and CB2 receptor-like immunoreactivity was found in Calu-3 cells. Subsequent pharmacological blockade of either cannabinoid receptor inhibited the THC effect. In comparison, stimulation of both or either CB1 or CB2 receptors displayed similar effect to that of THC. Western immunoblotting also revealed reproducible decreases in occludin and ZO-1 expression in TNFα-treated cells, whereas cells pre-incubated with THC alone or in combination with TNFα did not alter expression levels. Phosphorylation of myosin-phosphatase target protein at threonine 696 residue by TNFα was attenuated in the presence of THC, indicating the involvement of RhoA/ROCK cascade. Selective stimulation of either cannabinoid receptor in TNFα-treated cells suggests THC-induced inhibitory effect on RhoA/ROCK signalling was mediated through CB2 receptor, and not CB1. In summary, these data suggest that the reduction in transepithelial resistance by anandamide, indicative of increased epithelial permeability, is caused by its metabolites rather than anandamide itself. Inhibition of anandamide degradation might provide a novel approach to treat airway inflammation. Conversely, THC reverses the reduction in transepithelial resistance caused by TNFα, through an effect at CB1 and CB2 receptors. Hence, THC, or perhaps other cannabinoid receptor ligands may have potential therapeutic roles in inflammation-induced changes in airway epithelial cell permeability, such as asthma and COPD.
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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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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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Yi, Sheng. "Synthetic peptides modulate epithelial junctions." Thesis, Manhattan, Kan. : Kansas State University, 2009. http://hdl.handle.net/2097/2344.

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Elghadban, Salma. "Role of matriptase in the regulation of epithelial barrier permeability studied using MDCK cells." Thesis, University of East Anglia, 2014. https://ueaeprints.uea.ac.uk/53377/.

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The typeNII transmembrane serine protease matriptase plays an important role in the integrity of epithelial barriers. However, the molecular mechanisms underlying the role of matriptase are unknown. To study these mechanisms, two variants of MadinNDarby canine kidney (MDCK) cells were used, together with the “calciumNswitch” model of epithelial function with measurements of transepithelial electrical resistance (TEER). Inhibitors of matriptase proteolytic activity delayed the restoration of TEER after calciumNswitch in MDCKNI, which develop high TEER and lack the “leaky” tight junction protein claudinN2, but not MDCKNII. This effect was confirmed in MDCKNI, established to stably express matriptase targeted shRNA. The influence of matriptase inhibition on MDCKNI was shown not to involve altered expression or assembly of relevant components of paracelluar junctions or cytoskeleton. This excluded a role for claudinN2 in the function of matriptase, which had previously been shown in human CacoN2 cells, and this was confirmed using MDCKNI cells stably overexpressing claudinN2. To investigate the claudinN2Nindependent function of matriptase, a candidate substrate approach was used. Proteolytic activation of proNHGF/cNMet, PARN2, ENaC, EGFR and prostasin by matriptase has effects on epithelial cell function, but none were found to have a role in matriptase restoration of TEER after calciumN switch in MDCKNI cells. As the direct proteolytic target of matriptase could not be identified, potential mediators were studied using arrays for phosphorylated signalling proteins and inflammatory cytokines. ILN1β and complement component C5 were identified as genes downregulated by matriptase inhibition, while ILN13 showed upregulation. This work has confirmed the key role of matriptase activity in regulating epithelial barrier integrity. The differential properties of MDCKNI and MDCKNII cells excluded a role for claudinN2. None of the known proteolytic targets of matriptase were involved, however, changes in cytokine gene expression may be a potential route for matriptase effects on epithelial barrier maintenance.
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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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Viljoen, Ianda. "The role of surfactant in, and a comparison of, the permeability of porcine and human epithelia to various chemical compounds." Thesis, Link to the online version, 2005. http://hdl.handle.net/10019/1287.

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Books on the topic "Epithelial permeability"

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Compeau, Christopher Gary. Endotoxin-stimulated alveolar macrophages impair distal lung epithelial permeability and ion transport. Ottawa: National Library of Canada, 1994.

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R, Riordan John, Buchwald Manuel, and Canadian Cystic Fibrosis Foundation, eds. Genetics and epithelial cell dysfunction in cystic fibrosis: Proceedings of a symposium held in Kimberly, Ontario, Canada, November 12-15, 1986. New York: Liss, 1987.

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Ware, Lorraine B. Pathophysiology of acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0108.

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The acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure characterized by the acute onset of non-cardiogenic pulmonary oedema due to increased lung endothelial and alveolar epithelial permeability. Common predisposing clinical conditions include sepsis, pneumonia, severe traumatic injury, and aspiration of gastric contents. Environmental factors, such as alcohol abuse and cigarette smoke exposure may increase the risk of developing ARDS in those at risk. Pathologically, ARDS is characterized by diffuse alveolar damage with neutrophilic alveolitis, haemorrhage, hyaline membrane formation, and pulmonary oedema. A variety of cellular and molecular mechanisms contribute to the pathophysiology of ARDS, including exuberant inflammation, neutrophil recruitment and activation, oxidant injury, endothelial activation and injury, lung epithelial injury and/or necrosis, and activation of coagulation in the airspace. Mechanical ventilation can exacerbate lung inflammation and injury, particularly if delivered with high tidal volumes and/or pressures. Resolution of ARDS is complex and requires coordinated activation of multiple resolution pathways that include alveolar epithelial repair, clearance of pulmonary oedema through active ion transport, apoptosis, and clearance of intra-alveolar neutrophils, resolution of inflammation and fibrinolysis of fibrin-rich hyaline membranes. In some patients, activation of profibrotic pathways leads to significant lung fibrosis with resultant prolonged respiratory failure and failure of resolution.
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McAuley, Danny F., and Thelma Rose Craig. Measurement of extravascular lung water in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0140.

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The accumulation of fluid in the interstitium and alveolar space is known as extravascular lung water (EVLW). EVLW is associated with increased morbidity and mortality in critically ill patients and is elevated in patients with cardiogenic pulmonary oedema, acute lung injury (ALI), and the acute respiratory distress syndrome (ARDS). Pulmonary oedema is a consequence of increased pulmonary capillary hydrostatic pressure and/or an increased capillary permeability. The quantity of pulmonary oedema fluid is dependent on the balance of fluid formation and clearance, and this contributes to the overall dynamic net lung fluid balance. Measurement of EVLW is therefore an indirect surrogate measurement of the alveolar epithelial and endothelial damage in ALI/ARDS. The single indicator transpulmonary thermodilution technique is an available bedside technique to measure EVLW.
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White, Erin Marie. Permeability characteristics of the sea urchin blastula epithelium. 2002.

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Turner, Neil, and Premil Rajakrishna. Pathophysiology of oedema in nephrotic syndrome. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0053.

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The mechanism by which loss of serum proteins into the urine causes expansion of extracellular fluid volume and oedema has become clearer. A key initiating abnormality is avid sodium retention by the kidney, leading to increased whole-body sodium and increased extracellular fluid volume. This appears to be driven primarily by overactivation of the amiloride-sensitive epithelial sodium channel (ENaC) in the collecting duct, activated proteolytically through abnormal filtration of plasminogen, and its activation to plasmin in the nephron. Conventional explanations for nephrotic oedema focused on low colloid osmotic pressure as a consequence of loss of serum proteins, leading to egress of extracellular fluid from the intravascular compartment. It was hypothesized that this led to underfilling of the circulation and a drive to sodium retention. While low osmotic pressure may play a part in the clinical picture of nephrotic syndrome, a variety of observations suggest that underfilling is not a common feature except in the most severe nephrotic syndrome. Furthermore the gradient in colloid osmotic pressure between serum and interstitium tends to be preserved in nephrotic syndrome. The distribution of excess extracellular fluid is markedly different in patients with nephrotic syndrome from that seen in patients who have reduced glomerular filtration rate as the cause of sodium retention. This is not fully understood but hypotheses centre on capillary permeability and colloid osmotic pressure effects.
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Book chapters on the topic "Epithelial permeability"

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Wells, C. L., and S. L. Erlandsen. "Bacterial Translocation: Intestinal Epithelial Permeability." In Update in Intensive Care and Emergency Medicine, 131–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80224-9_9.

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Todisco, Tommaso, and Maurizio Dottorini. "Pulmonary epithelial permeability in adult RDS." In The Surfactant System of the Lung, 191–97. London: Macmillan Education UK, 1991. http://dx.doi.org/10.1007/978-1-349-12553-1_31.

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Benitez-del-Castillo, Jose M., Concha Aranguez, and Julian Garcia-Sanchez. "Corneal Epithelial Permeability and Dry Eye Treatment." In Advances in Experimental Medicine and Biology, 703–6. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0717-8_98.

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Vidyasagar, Sadasivan, and Gordon MacGregor. "Ussing Chamber Technique to Measure Intestinal Epithelial Permeability." In Methods in Molecular Biology, 49–61. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3603-8_6.

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Yüksel, Hasan, and Merve Öcalan. "Measurement of Airway Epithelial Permeability: Methods and Protocols." In Methods in Molecular Biology, 149–63. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/7651_2021_365.

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Donato, Rino P., Adaweyah El-Merhibi, Batjargal Gundsambuu, Kai Yan Mak, Emma R. Formosa, Xian Wang, Catherine A. Abbott, and Barry C. Powell. "Studying Permeability in a Commonly Used Epithelial Cell Line: T84 Intestinal Epithelial Cells." In Methods in Molecular Biology, 115–37. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-191-8_8.

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Larsen, Erik Hviid, and Jens Nørkær Sørensen. "Stationary and Nonstationary Ion and Water Flux Interactions in Kidney Proximal Tubule: Mathematical Analysis of Isosmotic Transport by a Minimalistic Model." In Reviews of Physiology, Biochemistry and Pharmacology, 101–47. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/112_2019_16.

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AbstractOur mathematical model of epithelial transport (Larsen et al. Acta Physiol. 195:171–186, 2009) is extended by equations for currents and conductance of apical SGLT2. With independent variables of the physiological parameter space, the model reproduces intracellular solute concentrations, ion and water fluxes, and electrophysiology of proximal convoluted tubule. The following were shown: Water flux is given by active Na+ flux into lateral spaces, while osmolarity of absorbed fluid depends on osmotic permeability of apical membranes. Following aquaporin “knock-out,” water uptake is not reduced but redirected to the paracellular pathway. Reported decrease in epithelial water uptake in aquaporin-1 knock-out mouse is caused by downregulation of active Na+ absorption. Luminal glucose stimulates Na+ uptake by instantaneous depolarization-induced pump activity (“cross-talk”) and delayed stimulation because of slow rise in intracellular [Na+]. Rate of fluid absorption and flux of active K+ absorption would have to be attuned at epithelial cell level for the [K+] of the absorbate being in the physiological range of interstitial [K+]. Following unilateral osmotic perturbation, time course of water fluxes between intraepithelial compartments provides physical explanation for the transepithelial osmotic permeability being orders of magnitude smaller than cell membranes’ osmotic permeability. Fluid absorption is always hyperosmotic to bath. Deviation from isosmotic absorption is increased in presence of glucose contrasting experimental studies showing isosmotic transport being independent of glucose uptake. For achieving isosmotic transport, the cost of Na+ recirculation is predicted to be but a few percent of the energy consumption of Na+/K+ pumps.
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Yu, Alan S. L. "Electrophysiological Characterization of Claudin Ion Permeability Using Stably Transfected Epithelial Cell Lines." In Methods in Molecular Biology, 27–41. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-185-7_3.

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Pfaller, W., M. Krall, H. Schramek, and M. P. Ryan. "Type I interferons increase paracellular permeability of renal epithelial cells in vitro." In Ersatz- und Ergänzungsmethoden zu Tierversuchen, 281–82. Vienna: Springer Vienna, 1998. http://dx.doi.org/10.1007/978-3-7091-7500-2_60.

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Smith, Prestina, Lauren A. Jeffers, and Michael Koval. "Measurement of Lung Vessel and Epithelial Permeability In Vivo with Evans Blue." In Methods in Molecular Biology, 137–48. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/7651_2020_345.

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Conference papers on the topic "Epithelial permeability"

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Hansi, R. K., G. K. Singhera, T. Shaipanich, D. D. Sin, D. R. Dorscheid, and J. M. Leung. "Respiratory Syncytial Virus Induces Epithelial Permeability in COPD and HIV Airway Epithelium." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3650.

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Song, Hyun-Ah, Yoon Ju Kim, Chang-Hoon Kim, and Joo-Heon Yoon. "Regulation Of Epithelial Permeability Via Hypoxia-HIF-1a-VEGF Axis In Airway Epithelia." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4214.

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Powdrill, JG, R. Ellis, JN Wattie, and MD Inman. "Effects of Inhaled Allergen on Epithelial Permeability and Hypersensitivity." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6041.

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Monzon, Maria E., Rosanna Malbran Forteza, and S. Marina Casalino-Matsuda. "Role Of Hyaluronan Fragments In The Regulation Of Epithelial Permeability." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5114.

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Sendon, C., C. DiPietro, H. Oez, C. Barone, R. Pierce, M. E. Egan, and E. M. Bruscia. "Electric Cell- Substrate Impedance Sensing Reveals Defective Permeability in Cystic Fibrosis Bronchial Epithelial Cells." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6192.

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Yilmaz, O., F. Odabasi Cingoz, B. Yilmaz, and H. Yuksel. "Influence of Epithelial Permeability on Long Term Airway Resistance in Children with Acute Wheezing." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6731.

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Thompson, Louise, Andra Vaida, Barry Campbell, and Carrie Duckworth. "OTH-001 Gliadin peptide P56–68 enhances epithelial permeability in a 3D enteroid model." In British Society of Gastroenterology, Annual General Meeting, 4–7 June 2018, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-bsgabstracts.323.

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Englert, JA, J. Ma, MA Perrella, and LE Fredenburgh. "COX-2 Deficiency Leads to Increased Intestinal Epithelial Permeability during Peritonitis-Induced Polymicrobial Sepsis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1144.

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Saffarzadeh, Mona, Muhammad Aslam, Christiane Juenemann, and Klaus T. Preissner. "The Role Of Neutrophil Extracellular Trap (NET) In Lung Epithelial Cell Cytotoxicity And Permeability." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2894.

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Raby, K., P. Dixey, N. Zounemat Kermani, J. Koranteng, F. Chung, and P. Bhavsar. "Mechanisms of nasal epithelial cell permeability in eosinophilic Severe Asthma: effect of anti-IL5R therapy." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.3938.

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