Relevant bibliographies by topics / Lung epithelial barrier function

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Lung epithelial barrier function'

Author: Grafiati
Published: 15 February 2024

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Journal articles on the topic "Lung epithelial barrier function"

1

Brune, Kieran, James Frank, Andreas Schwingshackl, James Finigan, and Venkataramana K. Sidhaye. "Pulmonary epithelial barrier function: some new players and mechanisms." American Journal of Physiology-Lung Cellular and Molecular Physiology 308, no. 8 (April 15, 2015): L731—L745. http://dx.doi.org/10.1152/ajplung.00309.2014.

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The pulmonary epithelium serves as a barrier to prevent access of the inspired luminal contents to the subepithelium. In addition, the epithelium dictates the initial responses of the lung to both infectious and noninfectious stimuli. One mechanism by which the epithelium does this is by coordinating transport of diffusible molecules across the epithelial barrier, both through the cell and between cells. In this review, we will discuss a few emerging paradigms of permeability changes through altered ion transport and paracellular regulation by which the epithelium gates its response to potentially detrimental luminal stimuli. This review is a summary of talks presented during a symposium in Experimental Biology geared toward novel and less recognized methods of epithelial barrier regulation. First, we will discuss mechanisms of dynamic regulation of cell-cell contacts in the context of repetitive exposure to inhaled infectious and noninfectious insults. In the second section, we will briefly discuss mechanisms of transcellular ion homeostasis specifically focused on the role of claudins and paracellular ion-channel regulation in chronic barrier dysfunction. In the next section, we will address transcellular ion transport and highlight the role of Trek-1 in epithelial responses to lung injury. In the final section, we will outline the role of epithelial growth receptor in barrier regulation in baseline, acute lung injury, and airway disease. We will then end with a summary of mechanisms of epithelial control as well as discuss emerging paradigms of the epithelium role in shifting between a structural element that maintains tight cell-cell adhesion to a cell that initiates and participates in immune responses.
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Aghapour, Mahyar, Alexander H. V. Remels, Simon D. Pouwels, Dunja Bruder, Pieter S. Hiemstra, Suzanne M. Cloonan, and Irene H. Heijink. "Mitochondria: at the crossroads of regulating lung epithelial cell function in chronic obstructive pulmonary disease." American Journal of Physiology-Lung Cellular and Molecular Physiology 318, no. 1 (January 1, 2020): L149—L164. http://dx.doi.org/10.1152/ajplung.00329.2019.

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Disturbances in mitochondrial structure and function in lung epithelial cells have been implicated in the pathogenesis of various lung diseases, including chronic obstructive pulmonary disease (COPD). Such disturbances affect not only cellular energy metabolism but also alter a range of indispensable cellular homeostatic functions in which mitochondria are known to be involved. These range from cellular differentiation, cell death pathways, and cellular remodeling to physical barrier function and innate immunity, all of which are known to be impacted by exposure to cigarette smoke and have been linked to COPD pathogenesis. Next to their well-established role as the first physical frontline against external insults, lung epithelial cells are immunologically active. Malfunctioning epithelial cells with defective mitochondria are unable to maintain homeostasis and respond adequately to further stress or injury, which may ultimately shape the phenotype of lung diseases. In this review, we provide a comprehensive overview of the impact of cigarette smoke on the development of mitochondrial dysfunction in the lung epithelium and highlight the consequences for cell function, innate immune responses, epithelial remodeling, and epithelial barrier function in COPD. We also discuss the applicability and potential therapeutic value of recently proposed strategies for the restoration of mitochondrial function in the treatment of COPD.
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Hollenhorst, Monika I., Katrin Richter, and Martin Fronius. "Ion Transport by Pulmonary Epithelia." Journal of Biomedicine and Biotechnology 2011 (2011): 1–16. http://dx.doi.org/10.1155/2011/174306.

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The lung surface of air-breathing vertebrates is formed by a continuous epithelium that is covered by a fluid layer. In the airways, this epithelium is largely pseudostratified consisting of diverse cell types such as ciliated cells, goblet cells, and undifferentiated basal cells, whereas the alveolar epithelium consists of alveolar type I and alveolar type II cells. Regulation and maintenance of the volume and viscosity of the fluid layer covering the epithelium is one of the most important functions of the epithelial barrier that forms the outer surface area of the lungs. Therefore, the epithelial cells are equipped with a wide variety of ion transport proteins, among which Na+, Cl−, and K+channels have been identified to play a role in the regulation of the fluid layer. Malfunctions of pulmonary epithelial ion transport processes and, thus, impairment of the liquid balance in our lungs is associated with severe diseases, such as cystic fibrosis and pulmonary oedema. Due to the important role of pulmonary epithelial ion transport processes for proper lung function, the present paper summarizes the recent findings about composition, function, and ion transport properties of the airway epithelium as well as of the alveolar epithelium.
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Herrero, Raquel, Mishie Tanino, Lincoln S. Smith, Osamu Kajikawa, Venus A. Wong, Steve Mongovin, Gustavo Matute-Bello, and Thomas R. Martin. "The Fas/FasL pathway impairs the alveolar fluid clearance in mouse lungs." American Journal of Physiology-Lung Cellular and Molecular Physiology 305, no. 5 (September 1, 2013): L377—L388. http://dx.doi.org/10.1152/ajplung.00271.2012.

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Alveolar epithelial damage is a critical event that leads to protein-rich edema in acute lung injury (ALI), but the mechanisms leading to epithelial damage are not completely understood. Cell death by necrosis and apoptosis occurs in alveolar epithelial cells in the lungs of patients with ALI. Fas activation induces apoptosis of alveolar epithelial cells, but its role in the formation of lung edema is unclear. The main goal of this study was to determine whether activation of the Fas/Fas ligand pathway in the lungs could alter the function of the lung epithelium, and the mechanisms involved. The results show that Fas activation alters the alveolar barrier integrity and impairs the ability of the lung alveolar epithelium to reabsorb fluid from the air spaces. This result was dependent on the presence of a normal Fas receptor and was not affected by inflammation induced by Fas activation. Alteration of the fluid transport properties of the alveolar epithelium was partially restored by β-adrenergic stimulation. Fas activation also caused apoptosis of alveolar endothelial cells, but this effect was less pronounced than the effect on the alveolar epithelium. Thus, activation of the Fas pathway impairs alveolar epithelial function in mouse lungs by mechanisms involving caspase-dependent apoptosis, suggesting that targeting apoptotic pathways could reduce the formation of lung edema in ALI.
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Kim, Kwang-Jin, and Asrar B. Malik. "Protein transport across the lung epithelial barrier." American Journal of Physiology-Lung Cellular and Molecular Physiology 284, no. 2 (February 1, 2003): L247—L259. http://dx.doi.org/10.1152/ajplung.00235.2002.

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Alveolar lining fluid normally contains proteins of important physiological, antioxidant, and mucosal defense functions [such as albumin, immunoglobulin G (IgG), secretory IgA, transferrin, and ceruloplasmin]. Because concentrations of plasma proteins in alveolar fluid can increase in injured lungs (such as with permeability edema and inflammation), understanding how alveolar epithelium handles protein transport is needed to develop therapeutic measures to restore alveolar homeostasis. This review provides an update on recent findings on protein transport across the alveolar epithelial barrier. The use of primary cultured rat alveolar epithelial cell monolayers (that exhibit phenotypic and morphological traits of in vivo alveolar epithelial type I cells) has shown that albumin and IgG are absorbed via saturable processes at rates greater than those predicted by passive diffusional mechanisms. In contrast, secretory component, the extracellular portion of the polymeric immunoglobulin receptor, is secreted into alveolar fluid. Transcytosis involving caveolae and clathrin-coated pits is likely the main route of alveolar epithelial protein transport, although relative contributions of these internalization steps to overall protein handling of alveolar epithelium remain to be determined. The specific pathways and regulatory mechanisms responsible for translocation of proteins across lung alveolar epithelium and regulation of the cognate receptors (e.g., 60-kDa albumin binding protein and IgG binding FcRn) expressed in alveolar epithelium need to be elucidated.
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Bao, Shenying, and Daren L. Knoell. "Zinc modulates cytokine-induced lung epithelial cell barrier permeability." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 6 (December 2006): L1132—L1141. http://dx.doi.org/10.1152/ajplung.00207.2006.

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Apoptosis plays a causative role in acute lung injury in part due to epithelial cell loss. We recently reported that zinc protects the lung epithelium during inflammatory stress whereas depletion of intracellular zinc enhances extrinsic apoptosis. In this investigation, we evaluated the relationship between zinc, caspase-3, and cell-to-cell contact via proteins that form the adherens junction complex. Cell adhesion proteins are directly responsible for formation of the mechanical barrier of the lung epithelium. We hypothesized that exposure to inflammatory cytokines, in conjunction with zinc deprivation, would induce caspase-3, leading to degradation of junction proteins, loss of cell-to-cell contact, and compromised barrier function. Primary human upper airway and type I/II alveolar epithelial cultures were obtained from multiple donors and exposed to inflammatory stimuli that provoke extrinsic apoptosis in addition to depletion of intracellular zinc. We observed that zinc deprivation combined with tumor necrosis factor-α, interferon-γ, and Fas receptor ligation accelerates caspase-3 activation, proteolysis of E-cadherin and β-catenin, and cellular apoptosis, leading to increased paracellular leak across monolayers of both upper airway and alveolar lung epithelial cultures. Zinc supplementation inhibited apoptosis and paracellular leak, whereas caspase inhibition was less effective. We conclude that zinc is a vital factor in the lung epithelium that protects against death receptor-mediated apoptosis and barrier dysfunction. Furthermore, our findings suggest that although caspase-3 inhibition reduces lung epithelial apoptosis it does not prevent mechanical dysfunction. These findings facilitate future studies aimed at developing therapeutic strategies to prevent acute lung injury.
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Wu, Huijuan, and Nan Tang. "Stem cells in pulmonary alveolar regeneration." Development 148, no. 2 (January 15, 2021): dev193458. http://dx.doi.org/10.1242/dev.193458.

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ABSTRACTThe lungs are constantly exposed to the external environment and are therefore vulnerable to insults that can cause infection and injury. Maintaining the integrity and barrier function of the lung epithelium requires complex interactions of multiple cell lineages. Elucidating the cellular players and their regulation mechanisms provides fundamental information to deepen understanding about the responses and contributions of lung stem cells. This Review focuses on advances in our understanding of mammalian alveolar epithelial stem cell subpopulations and discusses insights about the regeneration-specific cell status of alveolar epithelial stem cells. We also consider how these advances can inform our understanding of post-injury lung repair processes and lung diseases.
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Overgaard, Christian E., Barbara Schlingmann, StevenClaude Dorsainvil White, Christina Ward, Xian Fan, Snehasikta Swarnakar, Lou Ann S. Brown, David M. Guidot, and Michael Koval. "The relative balance of GM-CSF and TGF-β1 regulates lung epithelial barrier function." American Journal of Physiology-Lung Cellular and Molecular Physiology 308, no. 12 (June 15, 2015): L1212—L1223. http://dx.doi.org/10.1152/ajplung.00042.2014.

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Lung barrier dysfunction is a cardinal feature of the acute respiratory distress syndrome (ARDS). Alcohol abuse, which increases the risk of ARDS two- to fourfold, induces transforming growth factor (TGF)-β1, which increases epithelial permeability and impairs granulocyte/macrophage colony-stimulating factor (GM-CSF)-dependent barrier integrity in experimental models. We hypothesized that the relative balance of GM-CSF and TGF-β1 signaling regulates lung epithelial barrier function. GM-CSF and TGF-β1 were tested separately and simultaneously for their effects on lung epithelial cell barrier function in vitro. TGF-β1 alone caused an ∼25% decrease in transepithelial resistance (TER), increased paracellular flux, and was associated with projections perpendicular to tight junctions (“spikes”) containing claudin-18 that colocalized with F-actin. In contrast, GM-CSF treatment induced an ∼20% increase in TER, decreased paracellular flux, and showed decreased colocalization of spike-associated claudin-18 with F-actin. When simultaneously administered to lung epithelial cells, GM-CSF antagonized the effects of TGF-β1 on epithelial barrier function in cultured cells. Given this, GM-CSF and TGF-β1 levels were measured in bronchoalveolar lavage (BAL) fluid from patients with ventilator-associated pneumonia and correlated with markers for pulmonary edema and patient outcome. In patient BAL fluid, protein markers of lung barrier dysfunction, serum α2-macroglobulin, and IgM levels were increased at lower ratios of GM-CSF/TGF-β1. Critically, patients who survived had significantly higher GM-CSF/TGF-β1 ratios than nonsurviving patients. This study provides experimental and clinical evidence that the relative balance between GM-CSF and TGF-β1 signaling is a key regulator of lung epithelial barrier function. The GM-CSF/TGF-β1 ratio in BAL fluid may provide a concentration-independent biomarker that can predict patient outcomes in ARDS.
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Mitchell, Leslie A., Christian E. Overgaard, Christina Ward, Susan S. Margulies, and Michael Koval. "Differential effects of claudin-3 and claudin-4 on alveolar epithelial barrier function." American Journal of Physiology-Lung Cellular and Molecular Physiology 301, no. 1 (July 2011): L40—L49. http://dx.doi.org/10.1152/ajplung.00299.2010.

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Alveolar barrier function depends critically on the claudin family tight junction proteins. Of the major claudins expressed by alveolar epithelial cells, claudin (Cldn)-3 and Cldn-4 are the most closely related by amino acid homology, yet they differ dramatically in the pattern of expression. Previously published reports have shown that Cldn-3 is predominantly expressed by type II alveolar epithelial cells; Cldn-4 is expressed throughout the alveolar epithelium and is specifically upregulated in response to acute lung injury. Using primary rat alveolar epithelial cells transduced with yellow fluorescent protein-tagged claudin constructs, we have identified roles for Cldn-3 and Cldn-4 in alveolar epithelial barrier function. Surprisingly, increasing expression of Cldn-3 decreased alveolar epithelial barrier function, as assessed by transepithelial resistance and dye flux measurements. Conversely, increasing Cldn-4 expression improved alveolar epithelial transepithelial resistance compared with control cells. Other alveolar epithelial tight junction proteins were largely unaffected by increased expression of Cldn-3 and Cldn-4. Taken together, these results demonstrate that, in the context of the alveolar epithelium, Cldn-3 and Cldn-4 have different effects on paracellular permeability, despite significant homology in their extracellular loop domains.
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Ishii, Mitsutoshi, Tomoshi Tsuchiya, Ryoichiro Doi, Yoichi Morofuji, Takashi Fujimoto, Hideki Muto, Takashi Suematsu, et al. "Increased In Vitro Intercellular Barrier Function of Lung Epithelial Cells Using Adipose-Derived Mesenchymal Stem/Stromal Cells." Pharmaceutics 13, no. 8 (August 16, 2021): 1264. http://dx.doi.org/10.3390/pharmaceutics13081264.

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With the emergence of coronavirus disease-2019, researchers have gained interest in the therapeutic efficacy of mesenchymal stem/stromal cells (MSCs) in acute respiratory distress syndrome; however, the mechanisms of the therapeutic effects of MSCs are unclear. We have previously reported that adipose-derived MSCs (AD-MSCs) strengthen the barrier function of the pulmonary vessels in scaffold-based bioengineered rat lungs. In this study, we evaluated whether AD-MSCs could enhance the intercellular barrier function of lung epithelial cells in vitro using a transwell coculture system. Transepithelial electrical resistance (TEER) measurements revealed that the peak TEER value was significantly higher in the AD-MSC coculture group than in the AD-MSC non-coculture group. Similarly, the permeability coefficient was significantly decreased in the AD-MSC coculture group compared to that in the AD-MSC non-coculture group. Immunostaining of insert membranes showed that zonula occuldens-1 expression was significantly high at cell junctions in the AD-MSC coculture group. Moreover, cell junction-related gene profiling showed that the expression of some claudin genes, including claudin-4, was upregulated in the AD-MSC coculture group. Taken together, these results showed that AD-MSCs enhanced the barrier function between lung epithelial cells, suggesting that both direct adhesion and indirect paracrine effects strengthened the barrier function of lung alveolar epithelium in vitro.
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Dissertations / Theses on the topic "Lung epithelial barrier function"

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Zhai, Ruoyang. "Effects of sevoflurane in the treatment of Acute Respiratory Distress Syndrome : a translational approach." Electronic Thesis or Diss., Université Clermont Auvergne (2021-...), 2023. http://www.theses.fr/2023UCFA0077.

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Le syndrome de détresse respiratoire aiguë est une cause majeure d'insuffisance respiratoire avec un taux de mortalité élevé. Elle se caractérise par des lésions alvéolaires diffuses, un œdème alvéolaire et une défaillance respiratoire hypoxémique qui entraînent de lourds coûts de santé. Actuellement, les traitements disponibles pour le SDRA restent principalement de soutien, et aucune approche pharmacologique n'est traduite avec succès en application clinique. Il existe deux processus majeurs au cours du développement physiopathologique du SDRA qui conduisent à la formation d'un œdème pulmonaire :dysfonctionnement de la barrière alvéolaire et altération de la clairance du liquide alvéolaire suite à une lésion épithéliale alvéolaire et à une inflammation. Il a été indiqué que le récepteur des produits de glycation avancée (RAGE) était impliqué au cours de ces processus, avec le potentiel élevé de sa forme soluble en tant que biomarqueur pour le diagnostic et le pronostic du SDRA. Les agents halogénés volatils, tels que le sévoflurane ou l'isoflurane, sont de plus en plus utilisés dans les unités de soins intensifs comme agents sédatifs avec leurs caractéristiques intrinsèques idéales en tant que sédatifs. De plus, de nombreuses études précliniques et cliniques indiquent ses effets protecteurs pulmonaires chez les patients atteints de SDRA.Cependant, les mécanismes de ces effets bénéfiques restent à clarifier.Les principaux objectifs de ce travail de thèse sont multiples, à travers des approches expérimentales et modèles translationnels in vivo et in vitro du SDRA,1) Évaluer les effets protecteurs pulmonaires bénéfiques du sévoflurane dans le SDRA, y compris ses effets sur les caractéristiques physiologiques du SDRA, la clairance du liquide pulmonaire et la perméabilité alvéolaire.2) Étudier le mécanisme précis des effets observés du sévoflurane, y compris des études mécanistiques et la fonction et l'expression des protéines impliquées.3) Explorer le rôle de RAGE dans les lésions et la réparation de l'épithélium pulmonaire et son éventuel rôle de médiation des effets bénéfiques du sévoflurane.Au cours de ce travail de thèse, nous avons avancé sous plusieurs angles : Premièrement, nos travaux ont trouvé dans notre modèle de cicatrisation des cellules A549, le rôle important de RAGE dans la réparation des lésions pulmonaires processus, car son ligand, HMGB1, et les AGE ont favorisé la cicatrisation des plaies dépendante de RAGE des cellules épithéliales alvéolaires pulmonaires, ce qui est possiblement expliqué par une migration et une prolifération cellulaires améliorées. Deuxièmement, nos travaux sur des modèles murins de SDRA, trouve une diminution des indices de perméabilité et des structures épithéliales préservées dans les cellules et les souris, au moins en partie, augmentant l'expression de ZO-1 et l'inhibition de l'activité de RhoA et de pMLC ainsi que le réarrangement du cytosquelette d'actine suite à une lésion épithéliale pulmonaire . De plus, RAGE peut jouer un rôle médiateur dans les effets du sévoflurane sur les lésions pulmonaires aiguës. De plus, nos travaux sur des modèles de SDRA porcins in vivo ont confirmé les effets protecteurs pulmonaires du sévoflurane sur les caractéristiques du SDRA, avec une oxygénation améliorée, une perméabilité alvéolaire restaurée et une AFC améliorée. Notre étude suggère que l'effet protecteur du sévoflurane sur l'AFC peut s'expliquer par la restauration de l'expression pulmonaire altérée des canaux épithéliaux AQP-5, Na, K, ATPase et ENaC pendant le SDRA.Dans l'ensemble, ces travaux de thèse expliquent plus précisément les effets protecteurs des agents halogénés et la nouvelle révélation de son mécanisme potentiel, et conforte ainsi le grand intérêt pour l'utilisation de la sédation inhalée en soins intensifs pour les patients atteints de SDRA. Ce travail pourrait donner de nouvelles perspectives pour la recherche sur les effets du sévoflurane sur le SDRA et sa résolution
Acute respiratory distress syndrome (ARDS) is a major cause of respiratory failurewith a high mortality rate. It is characterized by diffuse alveolar damage, alveolar edema, and hypoxemic respiratory loss which cause heavy healthcare costs. Currently, available treatments for ARDS remain primarily supportive, and no pharmacological approach is successfully translated into clinical application. There are two major processes during the physiopathological development of ARDS that lead to the formation of lung edema:alveolar barrier dysfunction and the impairment of alveolar fluid clearance following alveolar epithelial injury and inflammation. The receptor for advanced glycation end products (RAGE) was indicated to be involved during those processes, with the high potential of its soluble form as a biomarker for ARDS diagnostic and prognostic. Volatile halogenated agents, such as sevoflurane or isoflurane, are increasingly used in intensive care units as sedative agents with their ideal intrinsic characteristics as a sedative. Furthermore, numerous pre-clinical and clinical studies indicate its lung protective effects for ARDS patients.However, its mechanisms of such beneficial effects remain to be clarified.The main objectives of this thesis work are multiple, through experimental andtranslational in vivo and in vitro models of ARDS, to1) Asses the beneficial lung protective effects of sevoflurane in ARDS, including its effects on ARDS physiological features, lung fluid clearance, and alveolar permeability.2) Investigate the precise mechanism of observed effects of sevoflurane, including mechanistic studies and involved proteins' function and expression.3) Explore the role of RAGE in lung epithelial injury and repair and its eventualmediation role of the beneficial effects of sevoflurane.During this thesis work, we advanced from many angles: First, our work found in ourA549 cells wound healing model, the important role of RAGE in the lung injury repairprocess, as its ligand, HMGB1, and AGEs promoted RAGE-dependent wound healing oflung alveolar epithelial cells, which is possible through enhanced cell migration and proliferation.Secondly, our work in murine in vitro and in vivo ARDS models, animprovement of experimental features, with decreased indices of permeability and preserved epithelial structures in cells and mice, by at least in a part, increasing expression of ZO-1 and the inhibition of RhoA activity and pMLC as well as actin cytoskeleton rearrangement following lung epithelial injury. Additionally, RAGE may play a mediating role in the effects of sevoflurane on acute lung injury. Furthermore, our work in porcine in vivo ARDS models confirmed the lung protective effects of sevoflurane on ARDS features, with improved oxygenation, restored alveolar permeability, and improved AFC. Our study suggests theprotective effect of sevoflurane on AFC may be explained by the restoration of impaired lung expression of epithelial channels AQP-5, Na, K, ATPase, and ENaC during ARDS.Taken together, this thesis work explained more precisely the protective effects ofhalogenated agents and the new revelation of its potential mechanism, and hence supports the high interest in the use of inhaled sedation in intensive care for ARDS patients. This work may give some new insights for research on the effects of sevoflurane on ARDS and its resolution.Keywords: Acute respiratory distress syndrome; Sevoflurane; Lung epithelial barrierfunction; Lung wound repair; Alveolar fluid clearance; Epithelial channels: Junction proteins;Intracellular pathways; Receptor for advanced glycation end-products
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Bueti, Deanna. "Immunomodulatory cytokines regulate intestinal epithelial barrier function /." Title page and abstract only, 2003. http://web4.library.adelaide.edu.au/theses/09SB/09sbb9289.pdf.

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Kraft, Martin Rolf. "Giardia duodenalis - epithelial interaction and barrier function." Doctoral thesis, Humboldt-Universität zu Berlin, 2020. http://dx.doi.org/10.18452/21045.

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Die Durchfallerkrankung Giardiasis wird durch den Protisten Giardia duodenalis ausgelöst. Die Infektion erfolgt fäkal-oral, meist über kontaminiertes Trinkwasser. Der Parasit kolonisiert den oberen Bereich des Dünndarms und heftt sich an das Epithel, wodurch es die Krankheitsbeschwerden auslöst. Allerdings sind Details über die Mechanismen der Pathogenese unbekannt. Dazu kommt, dass der Ausgang einer Infektion fallspezifisch starken Schwankungen unterworfen ist, von selbst-limitierend bis chronisch und asymptomatischer Kolonisierung bis hin zur schweren Enteritis. Ein möglicher Pathomechanismus ist der Wegfall der Barrierefunktion des Dünndarmepithels, z.B. durch Beeinträchtigung von tight junctions oder Zelltod. In dieser Arbeit wurden Effekte von G. duodenalis auf in vitro Modellsysteme des humanen Dünndarmepithels untersucht. Dazu wurden hauptsächlich Daten über die Barrierefunktion sowohl von der weit verbreiteten Caco-2 Zelllinie, als auch über ein neu etabliertes humanes Dünndarmorganoidsystem, erhoben. Es konnte gezeigt werden, dass mehrere - mitunter in der Literatur als hochvirulent beschriebene - G. duodenalis Isolate zu keinerlei Beeinträchtigung der Barrierefunktion oder irgendeiner anderen untersuchten potenziellen Schädigung an zwei unterschiedlichen Caco-2 Zelllinien unter diversen Infektions- und Kulturbedingungen führte. Jedoch andererseits das neu entwickelte Dünndarmorganoidsystem mit pseudo-luminalem Medium TYI S 33 reproduzierbar die Zerstörung des Epithelmodells mit Zellverlust, Zelltod (apoptotisch und nicht-apoptotisch), Störung der tight junctions (Abbau und Dislokation von Claudinen und ZO-1) und den Verlust von Mikrovilli innerhalb ein bis zwei Tage nach Parasiteninfektion zeigen konnte. Zudem wurde das Auftauchen von ClCa-1-Signalen unter andauerndem Infektionsstress beobachtet, was die Differenzierung bzw. Metaplasie zu Becherzellen nahelegt, jedoch keine Wirtsreaktion auf die Gewebszerstörung zu sein scheint.
The protozoan parasite Giardia duodenalis is the etiological agent for the intestinal diarrheal disease giardiasis. Infections are acquired via the fecal-oral route, mostly via uptake of cysts from contaminated drinking water. The colonization of the hosts’ duodenum and upper jejunum and the attachment of Giardia trophozoites onto the epithelium is the cause of a variety of gastrointestinal complaints but the exact pathomechanisms are unknown. Furthermore, the outcome of Giardia infections varies greatly between individuals, ranging from self-limiting to chronic, and asymptomatic to severe enteritis. One proposed mechanism for the pathogenesis is the breakdown of intestinal barrier function, e.g. by tight junction impairment or induction of cell death. In this work, effects of G. duodenalis on in vitro models of the human small intestinal epithelium were investigated by studying mainly barrier-related properties and changes of widely used Caco-2 cells as well as newly established human small intestinal organoid-derived monolayers (ODMs). It could be shown that several isolates of G. duodenalis, some described as highly virulent, fail to induce barrier dysfunction or any other investigated pathological effect on two Caco-2 cell lines under various infection and culturing conditions. On the other side, by developing a new organoid-based model system and the use of luminal mock medium TYI-S-33, considerable epithelial disruption (including loss of cells), cell death (apoptosis and non-apoptotic), tight junction impairment (degradation and dislocation of claudins and ZO-1), and microvilli depletion reproducibly induced by G. duodenalis trophozoites between one and two days after infection could be observed. Moreover, emergence of ClCa-1 positive cells with ongoing parasite infections suggest epithelial differentiation or metaplasia towards goblet cells, which is furthermore not associated to tissue damage.
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Baker, Sarah Elizabeth. "Epithelial Sodium Channel Polymorphism Influences Lung Function." Diss., The University of Arizona, 2013. http://hdl.handle.net/10150/306770.

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Epithelial sodium channels (ENaC) are located throughout the epithelial lining of the respiratory tract and play a crucial role in ion and fluid homeostasis of the lungs. Increasing ENaC activity through stimulation of β₂-adrenergic receptors has been shown to increase sodium and fluid reabsorption from the airspace to the interstitial space. In cystic fibrosis lung disease there is a hyperabsorption of sodium through ENaC which results in dehydration of the airway surface liquid. Previous work has identified a common functional genetic variant of SCNN1A, the gene encoding the ENaC alpha-subunit. This variant manifests as an alanine to threonine substitution at amino acid 663 (T663), with the T663 variant resulting in a more active channel due to a greater number of channels in the membrane. We sought to determine the influence of the T663 variant on exhaled ions, pulmonary function, and the diffusing capacity of the lungs in healthy subjects as well as in patients with cystic fibrosis. We used exercise, which can increase endogenous epinephrine by up to 1000 fold at peak exercise, and albuterol, an exogenous β₂-adrenergic agonist, to stimulate ENaC activity. In healthy individuals we hypothesized that the T663 variant would be beneficial for lung function due to a greater fluid removal, which could improve gas transfer in a healthy lung. In the CF patients we predicted that the T663 variant would be detrimental to lung function due to an exaggerated absorption of sodium and drying/thickening of the mucus layer in the airways. Measurements of exhaled sodium were made in the healthy subjects at baseline, 30, 60, and 90 minutes post-albuterol administration. Subjects with the A663 variant had higher baseline exhaled sodium and a significant decrease in exhaled sodium by 90 minutes after β₂-adrenergic stimulation with albuterol, suggesting a removal of sodium from the airways. No changes in exhaled sodium were seen in the T663 variant in response to albuterol. In response to exercise the A663 variant had a greater increase in the diffusing capacity of the lung than the T663 variant, possibly due to differences in alveolar sodium and therefore fluid handling. Taken together, these results suggest that healthy humans with the A663 variant can increase ENaC activity in response to β₂-adrenergic stimulation, whereas individuals with the T663 variant have a diminished capacity for increasing ENaC activity in response to β₂-adrenergic stimulation. In CF patients, the T663 variant had significantly lower baseline pulmonary function, weight, and body mass index. In response to exercise, patients with the T663 variant had a greater increase in the diffusing capacity of the lungs, possibly due to purinergic inhibition of ENaC. Finally, we recruited additional CF patients to confirm our pulmonary function findings. Individuals with at least one allele resulting in the T663 variant had significantly lower body mass index, and tended to have lower exhaled chloride and pulmonary function. These results suggest greater dehydration of the lung in CF patients with the T663 variant. Overall, these results may suggest that the T663 variant modifies disease severity in CF, although more work is certainly warranted to confirm this result.
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Beltinger, Johannes Hermann. "Studies on colonic epithelial ion transport and barrier function." Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311747.

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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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Glymenaki, Maria. "The role of gut flora in epithelial barrier function and immunity." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-gut-flora-in-epithelial-barrier-function-and-immunity(6cb0ca1e-06ff-4cd4-a0a1-76ace6af2a55).html.

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Inflammatory bowel disease (IBD) is associated with an inappropriate immune response to the gut microbiota and disruption of intestinal homeostasis. IBD patients and experimental animal models have consistently shown alterations in the gut microbiota composition. However, these studies have mainly focused on faecal microbiota samples taken after the onset of inflammation and IBD establishment. The colonic microbiota inhabits both the gut lumen and the mucus layer covering the intestinal epithelium. Thus, information about mucus-resident microbiota is not necessarily conveyed in the routine microbiota analyses of faecal samples. To address potential changes in microbial composition and function before the onset of IBD, we compared both mucus and faecal microbiota in the mdr1a-/- spontaneous model of colitis over times that we histologically defined as before onset of colitis, during and after colitis onset. We showed that alterations in microbiota composition preceded the onset of intestinal inflammation and that these changes were evident in the mucus, but not in faeces. This altered microbiota composition was coupled with a reduced inner mucus layer, indicating a compromised mucus barrier prior to colitis development. Upon emergence of inflammation, compositional differences were found in both mucus and faecal microbial communities. Spatial segregation of microbiota with intestinal mucosa was also disrupted on disease onset which we hypothesise contributes to a more severe intestinal pathology. Therefore, our data indicate that microbial changes start locally in the mucus and then proceed to the faecal matter concomitantly with colitis development. Next, we examined whether microbial gene functional potential and endogenous metabolite profiles followed alterations in gut microbiota taxonomic composition. Our findings showed that the microbial gene content was similar between mdr1a-/- mice and wild-type littermate controls, demonstrating stability of the gut microbiome at the face of ensuing gut inflammation. In further support of these findings, urinary metabolite analysis revealed that metabolite profiles were unaffected by intestinal inflammation. Metabolites previously reported to change in IBD were similar between mdr1a-/- and wild-type mice at stages preceding and during inflammation. We also found that changes in metabolite profiles did not correlate with colitis scores. However, metabolite changes could discriminate mdr1a-/- mice from wild-type controls, suggesting they could have value in predicting risk of IBD with a potential clinical use in at least a subset of individuals with MDR1A polymorphisms. To assess whether changes in antimicrobial proteins (AMPs) accounted for observed differences in mucus microbiota composition, we also investigated the expression of regenerating islet-derived protein 3 γ (Reg3γ), angiogenin 4 (Ang4), β-defensin 1 and resistin-like molecule beta (Relm-β) in the colon. We found similar levels of these AMPs as well as IgA-producing plasma cells between mdr1a-/- and wild-type mice, suggesting that other factors contribute to alterations in microbiota composition. Overall, our data indicate that the mdr1a-/- is a good model of colitis, as it enables us to look at pre-clinical changes in the gut microbiota. This work suggests the importance of mucus sampling for sensitive detection of microbiota changes. Furthermore, metabolite profiling may be a helpful way to discriminate genetic susceptibility to disease.
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Roux, Jérémie. "Function of the epithelial sodium channel ENaC in acute lung injury." Nice, 2005. http://www.theses.fr/2005NICE4010.

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L’objectif de cette thèse est de mettre en évidence le rôle des canaux ioniques de l’épithélium alvéolaire dans la pathogenèse du syndrome de détresse respiratoire aiguë. Des études cliniques ont montré que l’absorption anormale de l’œdème pulmonaire par l’épithélium alvéolaire secondaire à la libération de médiateurs inflammatoires est une manifestation caractéristique du syndrome de détresse respiratoire aiguë. Dans une première étude, nous avons démontré que l’activité élevée du transforming growth factor -b1 (TGF-b1) présent dans les alvéoles lors de détresse respiratoire aiguë provoque un œdème pulmonaire en réduisant le transport vectoriel de sodium et de fluides à travers l’épithélium alvéolaire. Puis, nous avons montré que l’interleukine -1b (IL-1b) permet l’activation de TGF-b1 via un mécanisme cellulaire dépendant de l’intégrine avb6. Finalement, dans une dernière étude, nous avons montré que IL-1b affecte directement et indirectement le transport vectoriel de sodium et d’eau à travers l’épithélium alvéolaire. Cette réduction de transport de fluides s’est révélée être due en majeure partie à une diminution de la présence du canal sodium épithélial (ENaC) à la membrane apicale des cellules épithéliales alvéolaires, causée par l'inhibition de l’activité du promoteur d’ENaC par un mécanisme dépendant des MAP kinases. L’ensemble de ces études démontre que TGF-b1 et IL-1b affectent la biosynthèse d’ENaC, et suggère un rôle clé pour ces médiateurs dans la persistance de l'œdème pulmonaire chez les patients atteints de détresse respiratoire aiguë
The objective of this thesis is to investigate the role of abnormalities in alveolar epithelial ion channel function in the pathogenesis of acute lung injury. Clinical studies have demonstrated that impaired alveolar fluid clearance associated with the release of inflammatory mediators within the distal airspace of the lung is a characteristic feature of acute lung injury. Therefore, we examined the potential effect of these mediators on ion transport across the alveolar epithelium. In the first study, we demonstrated that increased transforming growth factor -b1 (TGF-b1) activity in distal airspaces during acute lung injury promoted pulmonary edema by reducing alveolar epithelial sodium and fluid transport. In the second study we showed that in alveolar epithelial cells, interleukin -1b (IL-1b) activated TGF-b1 via an integrin avb6-dependent mechanism. Finally in the last study, we demonstrated that IL-1b could also directly and independently reduce the alveolar epithelial sodium and fluid transport. The reduction in fluid transport was shown to be attributable in large part to a decrease in apical membrane expression of the epithelial sodium channel (ENaC) in lung epithelial cells. The decreased cell surface expression of ENaC was mediated through a MAP kinase-dependent inhibition of ENaC promoter activity. In summary, the studies presented here demonstrate that IL-1b and TGF-b1 down-regulate ENaC biosynthesis and indicate a critical role for these mediators in the impaired fluid clearance of patients with acute lung injury
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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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HU, Li-Li. "STAT3 in intestinal epithelial cells regulates barrier function and anti-bacterial response." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p1465075.

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Thesis (M.S.)--University of California, San Diego, 2009.
Title from first page of PDF file (viewed July 22, 2009). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 57-63).
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Books on the topic "Lung epithelial barrier function"

1

E, Patterson Carolyn, ed. Perspectives on lung endothelial barrier function. Amsterdam: Elsevier, 2005.

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Perspectives on Lung Endothelial Barrier Function. Elsevier, 2005. http://dx.doi.org/10.1016/s1569-2558(05)x3500-7.

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Patterson, C. E., and Edward Bittar. Perspectives on Lung Endothelial Barrier Function. Elsevier Science & Technology Books, 2004.

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Patterson, C. E. Perspectives on Lung Endothelial Barrier Function, Volume 35 (Advances in Molecular and Cell Biology). Elsevier Science, 2005.

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(Editor), Jorg-Dieter Schulzke, Michael Fromm (Editor), Ernst-Otto Riecken (Editor), and Henry J. Binder (Editor), eds. Epithelial Transport and Barrier Function: Pathomechanisms in Gastrointestinal Disorders (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2001.

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Schulzke, Jorg-Dieter. Epithelial Transport and Barrier Function: Pathomechanisms in Gastrointestinal Disorders (Annals of the New York Academy of Sciences, V. 915). New York Academy of Sciences, 2000.

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Elger, Marlies, and Wilhelm Kriz. The renal glomerulus. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0043.

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The glomerulus performs its functions with three major cell types. Endothelial cells and visceral epithelial cells (podocytes) lie on the inside and outside of the glomerular basement membrane, and together these three structures form the glomerular filtration barrier. Mesangial cells sit in the axial region. Pathologies of all these regions and cell types can be identified. Parietal epithelial cells lining Bowman’s capsule participate in crescent formation, and at the tubular pole some of these cells seem to represent a stem cell population for tubular cells and podocytes. The extraglomerular mesangium and juxtaglomerular apparatus complete the description of the glomerular corpuscle. The structure of these elements, and how they relate to function, are illustrated in detail.
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Snell, Jamey, and Thomas J. Mancuso. Cystic Fibrosis. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0023.

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Cystic fibrosis (CF) is an inherited, autosomal recessive, multisystem disease. Dysfunction of the cystic fibrosis transmembrane conductance regulator protein (CFTR) in epithelial cells is the primary defect in CF. Defects in CFTR are the cause for lung disease, exocrine pancreatic insufficiency and failure, male infertility, and liver disease. CF can present with a variety of respiratory and gastrointestinal signs, including meconium ileus in the newborn period, hypernatremic dehydration, pulmonary insufficiency, nasal polyps, and insulin-dependent diabetes mellitus. As affected children grow, dysfunction in CFTR leads to chronic and progressive lung disease, characterized by suppurative infection and the development of bronchiectasis. CFTR dysfunction also affects exocrine function, leading to pancreatic insufficiency, malabsorption, and growth failure. In the past, history and physical exam with sweat chloride testing were the cornerstones of diagnosis. Diagnosis is now made with the newborn screening test for immunoreactive trypsinogen.
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Harrois, Anatole, and Jacques Duranteau. Pathophysiology of severe capillary leak. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0164.

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Severe capillary leak plays an important role in the pathogenesis of several inflammatory syndromes, including sepsis, acute lung injury, and shock syndromes. Microvascular leak is caused by an increase in endothelial permeability. This is due to a range of inflammatory mediators that destabilize endothelial junctions, thereby causing tissue oedema with potential harmful effects on tissue oxygenation and organ function. Tissue oedema can impair tissue oxygenation by increasing the distance required for the diffusion of oxygen to cells, and by decreasing microvascular perfusion due to an increase in interstitial pressure. Better understanding of the pathogenesis of microvascular permeability may lead to new therapies targeting the microvascular barrier in sepsis and the acute respiratory distress syndrome.
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Patterson, Caroline, and Meg Coleman. Revision Notes for the Respiratory Medicine Specialty Certificate Examination. Oxford University Press, 2012. http://dx.doi.org/10.1093/oso/9780199693481.001.0001.

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The newly introduced Specialty Certificate Examinations are a compulsory component of assessment for all UK medical trainees and represent the final examination barrier before getting the certificate of completion of training. This book provides a unique exam-specific revision guide for the Respiratory specialty certificate exam. Comprising of best of five test multiple choice questions and revision notes to facilitate targeted study, Revision Notes for the Respiratory Medicine Specialty Certificate Examination is the only book you need to prepare for this important examination. Questions are based around clinical scenarios and supplemented with images of radiological investigations such as x-rays, and lung function tests. Each question is structured as in the exam itself. The second half of the book comprises of a series of tutorials covering key areas and difficult concepts assessed in the examination including respiratory infection, respiratory malignancy, industrial lung disease, sleep disorders, standard respiratory tests and medical statistics. The combined approach allows trainees to become acquainted with the "best of five" format and facilitate recognition of areas of weakness and targeted study.
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Book chapters on the topic "Lung epithelial barrier function"

1

Smith, Gideon P. "Normal Immune Function and Barrier: Epithelial Barrier." In Encyclopedia of Medical Immunology, 807–9. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_267.

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Matthay, M. A., T. Nuckton, and B. Daniel. "Alveolar Epithelial Barrier: Acute Lung Injury." In Yearbook of Intensive Care and Emergency Medicine, 189–205. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-662-13455-9_17.

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Strengert, Monika, and Ulla G. Knaus. "Analysis of Epithelial Barrier Integrity in Polarized Lung Epithelial Cells." In Methods in Molecular Biology, 195–206. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-191-8_13.

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Rios-Arce, Naiomy Deliz, Fraser L. Collins, Jonathan D. Schepper, Michael D. Steury, Sandi Raehtz, Heather Mallin, Danny T. Schoenherr, Narayanan Parameswaran, and Laura R. McCabe. "Epithelial Barrier Function in Gut-Bone Signaling." In Advances in Experimental Medicine and Biology, 151–83. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-66653-2_8.

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Madara, James L., Shirin Nash, Ronda Moore, Michael Shapiro, Susan Carlson, and Charlene Delp. "Barrier Function of Intestinal Epithelial Tight Junctions (TJ)." In Inflammatory Bowel Diseases 1990, 27–33. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1980-8_4.

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Ali, Shariq, and Erik Rytting. "Influences of Nanomaterials on the Barrier Function of Epithelial Cells." In Advances in Experimental Medicine and Biology, 45–54. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-8739-0_3.

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Kalifa, Lidza, and Michael A. O’Reilly. "The Impact of DNA Damage on Epithelial Cell Maintenance of the Lung." In Mitochondrial Function in Lung Health and Disease, 141–59. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0829-5_7.

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Matthay, M. A., G. Nitenberg, and C. Jayr. "The Critical Role of the Alveolar Epithelial Barrier in Acute Lung Injury." In Yearbook of Intensive Care and Emergency Medicine, 28–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79154-3_3.

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Paugh, Jerry R., Alan Sasai, and Abhay Joshi. "Preservative Effect on Epithelial Barrier Function Measured with a Novel Technique." In Lacrimal Gland, Tear Film, and Dry Eye Syndromes 2, 731–35. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5359-5_103.

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Stefanski, Adrianne L., Dorota S. Raclawska, and Christopher M. Evans. "Modulation of Lung Epithelial Cell Function Using Conditional and Inducible Transgenic Approaches." In Methods in Molecular Biology, 169–201. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8570-8_14.

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Conference papers on the topic "Lung epithelial barrier function"

1

Muizer, Kirsten, Maaike De Vries, Wim Timens, Maarten Van Den Berge, Alen Faiz, Tillie-Louise Hackett, Corry-Anke Brandsma, and Irene H. Heijink. "The effect of age on lung epithelial barrier function." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.oa2124.

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Chen, Q., M. De Vries, M. Boezen, and I. Heijink. "The role of the COPD susceptibility gene FAM13A in barrier function and pro-inflammatory responses of human airway epithelial cells." In ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.59.

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LaFemina, Michael J., Trevor Bentley, Katherine Sutherland, Deepti Rokkam, Lennell Allen, Leland G. Dobbs, and James Frank. "A Role For Lung-Specific Tight Junction Protein Claudin-18 In Alveolar Epithelial Barrier Function." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6740.

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Boland, Helena, Endres Adrian, Hans Schwarzbach, Anke Burger-Kentischer, Danny Jonigk, Peter Braubach, Gernot Rohde, and Carla Bellinghausen. "Protective effect of interferon type I on barrier function of human airway epithelium during rhinovirus infections in vitro." In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.92.

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Boland, H., A. Endres, A. Burger-Kentischer, D. Jonigk, P. Braubach, G. Rohde, and C. Bellinghausen. "Protective effect of interferon type I on barrier function of the human airway epithelium during rhinovirus infections in vitro." In ERS Lung Science Conference 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/23120541.lsc-2023.41.

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LaFemina, Michael J., Deepti Rokkam, Trevor M. Bentley, Michael A. Matthay, and James A. Frank. "Bronchoalveolar Lavage Fluid From Patients With Acute Lung Injury Alters Barrier Function In Primary Alveolar Epithelial Cell Monolayers." 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.a5096.

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Larsson, M., K. Balogh Sivars, M. Forsgard, M. Parsson, and J. Hornberg. "MEK/ERK Inhibitors Affect Epithelial Barrier Function in Cells with Ongoing Active Repair Processes Indicating a Potential Hazard in Patients with Healing Lung." 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.a5248.

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Xiao, Cathy, Sarah A. Field, Joel Haywood, Victoria Broughton-Head, Nicole Bedke, Catherine Cremin, Stephen T. Holgate, Sarah M. Puddicombe, Phillip Monk, and Donna E. Davies. "Defective Epithelial Barrier Function In Asthma." 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.a6367.

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Sidhaye, Venkataramana, Eric Chau, Patrick Breysse, and Landon S. King. "Particulate Matter Alters Airway Epithelial Barrier Function." 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.a6392.

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Greaney, A. M., M. S. B. Raredon, T. Adams, R. Langer, N. Kaminski, and L. E. Niklason. "Building Epithelial Barrier in Whole-lung Tissue Engineering." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a6159.

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Reports on the topic "Lung epithelial barrier function"

1

Michael Anderson, Michael Anderson. Trans-epithelial Electrical Resistance (TEER) device to study the circadian rhythms of intestinal barrier function. Experiment, May 2023. http://dx.doi.org/10.18258/51202.

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