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Tesi sul tema "Airway epithelium"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 6 luglio 2024

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1

Shebani, Eyman. "Ultrastructural Studies of the Airway Epithelium in Airway Diseases". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6632.

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2

Stevens, Paul. "Intrinsic differences of the airway epithelium in childhood allergic asthma". University of Western Australia. School of Paediatrics and Child Health, 2009. http://theses.library.uwa.edu.au/adt-WU2010.0022.

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[Truncated abstract] Asthma affects millions of people worldwide and places a substantial burden on the healthcare system. Despite advances in our understanding of disease mechanisms and the role of respiratory viruses in asthma exacerbations, there is little known regarding the role of the epithelium in commonly observed structural changes in the airway wall. The epithelium of the airways provides an essential protective barrier between the environment and underlying structures and is responsible for the secretion of diverse compounds. Since it is likely that dysregulated epithelial characteristics and function in childhood asthma are critical determinants of disease progression in adults, it is pertinent to investigate the cellular mechanisms involved in paediatric asthma. However, full comprehension of paediatric respiratory diseases and the childhood antecedents of adult respiratory disease are currently hampered by the difficulty in obtaining relevant target organ tissue and most of the data to date have been generated from studies involving adults or commercially derived cell lines. This laboratory has successfully developed methodologies of obtaining and studying samples of paediatric primary airway epithelial cells (pAECs) and has identified significant biochemical and functional differences between healthy non-atopic (pAECHNA) and atopic asthmatic (pAECAA) airway cells, which have assisted in the identification of potential mechanisms responsible for abnormal epithelial function. Stevens 2009 ... Exposure of pAECs with RV resulted in elevated PAI-1 mRNA expression and reduced MMP-9 release in both pAECAA and pAECHNA samples. Collectively, the data presented indicate that RV exposure induces a pronounced antiproliferative and retardative repair effect in pAECAA and that the presence of virus may have a role in the PAI-1 and MMP expression witnessed in these cells. In conclusion, this investigation has further characterised the essential role the airway epithelium plays in childhood asthma by demonstrating for the first time that pAECs from asthmatic children lack the ability to successfully repair mechanically induced wounds. This investigation also showed that PAI-1 is elevated in pAECAA and has a functional role in the pAEC proliferative and regenerative processes. It was demonstrated that MMP-2 and MMP-9 activities and the MMP-9/TIMP-1 as well as MMP2/TIMP2 ratios were significantly reduced in pAECAA thereby providing additional evidence that there is a dysregulation in the mechanisms that monitor the turnover of the ECM in childhood asthma. Furthermore, this study has shown for the first time that pAECs from untreated mild atopic-asthmatic children are more sensitive to the pathogenic effects of RV than healthy control cells and that RV exposure delays cellular proliferation and repair. Ultimately, these findings support the hypothesis postulated and provide evidence that indeed the dysregulated epithelial functional characteristics seen in childhood mild asthma may be a critical determinant of disease progression in adults.
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3

Scull, Margaret Adele Pickles Raymond J. "Myxovirus interaction with the human airway epithelium". Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2009. http://dc.lib.unc.edu/u?/etd,2848.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2009.
Title from electronic title page (viewed Jun. 4, 2010). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Microbiology and Immunology." Discipline: Microbiology and Immunology; Department/School: Medicine.
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4

Wang, Jiahua. "The role of airway epithelium in airway inflammation and effect of corticosteroids". Thesis, Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300175.

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5

Rowley, Jessica. "The interaction of Aspergillus fumigatus with the respiratory epithelium". Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/the-interaction-of-aspergillus-fumigatus-with-the-respiratory-epithelium(0fc10449-977d-4f14-a169-172e8204fee4).html.

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Aspergillus fumigatus is a filamentous fungus and the main pathogen responsible for the often fatal respiratory condition, aspergillosis. Airway epithelial cells (AECs) are likely to be the first line of host defence that come into contact with the inhaled conidia of A. fumigatus. Recent evidence strongly suggests that the response of the airway epithelium to inhaled pathogens is pivotal in orchestrating immune responses by inducing phagocytic-like reactions and the secretion of inflammatory cytokines and antimicrobial peptides. However, the majority of previous work investigating A. fumigatus-host interactions has been performed using macrophages and neutrophils, thereby neglecting the epithelium. AECs have been shown to secrete inflammatory cytokines in response to A. fumigatus although these studies predominantly used transformed AEC lines that lack tight junctions and do not fully differentiate. Furthermore, most studies used culture filtrate or extract of A. fumigatus rather than live, whole organism and as a result, the direct interaction of the germinating fungus and the airway epithelium has been overlooked. During the early germination and growth period, the cell wall composition of A. fumigatus is dynamic, with various antigens exposed at different morphological stages. The aim of this thesis was to determine whether AECsare able to alter the germination and growth rate of A. fumigatus, and, conversely, if A. fumigatus affects AECs in terms of the secretion of inflammatory mediators. These studies used live, germinating A. fumigatus, and human primary differentiated AECs to obtain a more realistic in vitro model than those used in previous studies. Data showed that AECs are able to significantly inhibit the germination and growth of A. fumigatus, although this effect was less pronounced in differentiated primary AEC than in transformed AEC lines. A. fumigatus also significantly inducedthe expression and secretion of the inflammatory cytokines, IL-6 and IL-8, probably via the interaction of fungal cell wall β-glucans, and as of yet unidentified AEC receptor. The A1160pyrG+ strain of A. fumigatus secreted factors capable of inducing cytokine secretion whereas Af293 strain did not, highlighting diverse mechanisms of action for different strains. Upregulation of both cytokines was dependent on the stage of A. fumigatus growth with induction synchronous with germination. Despite being associated with fungal sensitisation in asthmatics, AEC-derived cytokines associated with this disease, namely TSLP, IL33 and IL25,did not appear to be upregulated by transformed AECs in response to A. fumigatus. Similarly, A. fumigatus did not seem to induce synthesis and secretion of the acute phase response protein, fibrinogen above baseline levels. The data presented in this thesis confirms the importance of the airway epithelium in directing anti-A. fumigatus immunity and the involvement of complex ligand-receptor interactions.
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6

Fox, Emma. "Systemic delivery of DNA to the airway epithelium". Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409742.

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7

Leahy, Rachel A. "Signal Transduction and Cellular Differentiation in Airway Epithelium". Kent State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=kent1352673026.

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8

FORTNER, CHRISTOPHER NEIL. "EPITHELIUM-DEPENDENT RELAXATION OF AIRWAY SMOOTH MUSCLE IS LINKED TO EPITHELIAL CHLORIDE CURRENTS". University of Cincinnati / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ucin983467525.

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9

Williams, M. T. S. "Impact of different CFTR Mutations on Airway Epithelium Function". Thesis, Queen's University Belfast, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.527902.

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10

Jing, Yi. "Epithelial mechanisms in airway responses induced by hyperosmolarity". Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5054.

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Thesis (Ph. D.)--West Virginia University, 2007.
Title from document title page. Document formatted into pages; contains xiv, 155 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
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11

Nilsson, Harriet. "Studies of Tight Junctions and Airway Surface Liquid in Airway Epithelium with Relevance to Cystic Fibrosis". Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-99411.

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Cystic fibrosis (CF) is a multi-organ autosomal recessive disease of fluid-transporting epithelia, due to a mutation in the gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. CFTR is a cAMP-regulated Cl-channel involved in various regulatory processes. Salt and water transport depend on CFTR and the epithelial sodium channel (ENaC), operating in concert with the paracellular pathway through the tight junctions (TJ). The ionic composition of the ASL has been assumed to be altered in CF, resulting in a fatal accumulation of viscous mucus in the airways. ASL samples were collected from tracheal and nasal fluid in normal and transgenic CF mice and from the fluid covering the apical surface of normal bronchial cells (16HBE14o-) and a CF human bronchial cell line (CFBE41o-). Analysis of the elemental content of the ASL was performed by X-ray microanalysis. The ASL contained more Na and Cl in CFTR-deficient or DF508-CFTR-containing cells than in control cells with wild- type CFTR. The relation between osmolarity and TJ permeability was examined by the addition of salt or sugar (295-700 mOsm) to 16HBE14o- cells, where the integrity of TJ was evaluated by transepithelial electrical resistance (TEER) measurements. Studies of interaction between the activity of CFTR, TJ and cytoskeleton were performed in CFBE41o-, plasmid corrected CFBE41o- (CFBE41o pCep4), and 16HBE14o- cells exposed to an inhibitor of CFTR (CFTRinh-172). The TJ were investigated by determining the paracellular permeability to lanthanum ions or with [14C] mannitol. Cytoskeletal changes were evaluated by immunofluorescence. Hyperosmotic stress resulted in opening of TJ. Inhalation of hypertonic salt or sugar solutions may open TJ, leading to enhanced paracellular water transport and increased ASL volume, diluted mucus and enhanced mucociliary clearance. This may explain the beneficial effect of this treatment for CF-patients. In healthy airway epithelial cells, inhibition of CFTR by CFTRinh-172 resulted in an increased TEER, whereas stimulation of CFTR by IBMX/forskolin caused a decrease. The paracellular permeability was inversely proportional to TEER. Immunofluorescence revealed a disorganization of cytoskeletal proteins in CF-cells. These results point toward a possible interaction between the activity of CFTR and TJ protein complex, presumably via the cytoskeleton.
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12

Armit, Christopher James. "p53 and responses to DNA damage in small airway epithelium". Thesis, University of Edinburgh, 2001. http://hdl.handle.net/1842/27777.

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The effects of p53 were investigated in a mouse model of acute lung injury and in short-term primary cultures of isolated Clara cells. Gene targeted mice, germline deficient in p53, were exposed to γ-irradiation and compared to wild type controls. The in vivo response was to DNA damage was characterised in terms of growth arrest, apoptosis, morphology, and gene expression. An acute stress response was observed in vivo, and localised to a subpopulation of the lung epithelium, the bronchiolar cells. p53 was stabilised in this population and was associated with transcriptional induction of Bax, but not other bcl-2 family members. p53 deficient mice did not display this rapid accumulation of Bax transcripts, as assessed by RNase Protection Assay. Within wild type and p53 null mice, γ-irradiation did not induce apoptosis in lung epithelial cells at any timepoints studied, as assessed by morphology, but induce strand breaks that were detectable by TUNEL. Cell cycle activity as assessed by BrdU incorporation, was infrequent in the lung at all timepoints, regardless of p53 status, and hence an effect of p53 on cell cycle progression was not detected in vivo. The effects of p53-deficiency was additionally investigated in short-term primary cultures of murine bronchiolar Clara cells. Culturing of Clara cells allowed an assessment of the functional consequences of p53 deficiency in proliferating cells. Clara cells, isolated from gene-targeted p53-deficient mice, were compared to cells derived from wild type littermates. Baseline proliferation rates, as determined by BrdU incorporation, were similar irrespective of p53 status. p53 null cultures displayed abnormal morphology; specifically, a high incidence of multinucleation, which increased with time in culture. Multinucleated cells maintained expression of the Clara cell marker for CC10, and were proficient in S phase DNA synthesis, as determined by BrdU incorporation. Nucleation defects in p53 -/- Clara cells associated with abnormalities in mitosis and cytokinesis, as documented by time-lapse videomicroscopy, and with increased centrosome number, determined by confocal microscopy.
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13

Stefanowicz, Dorota. "Profiling the epigenetic landscape of the airway epithelium in asthma". Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/47071.

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The airway epithelium is the interface between the environment and the submucosa of the lung and thus is the first line of defense against inhaled exogenous agents. In addition to maintaining a structural barrier through homeostasis and repair, the airway epithelium is involved in co-ordination of the mucosal immune response to the inhaled environment. In asthma it is now understood that the airway epithelium is abnormal with dysregulation of genes integral to differentiation, proliferation, and inflammation. Alteration of the chromatin architecture through epigenetic modifications including DNA methylation and histone modifications is reactive to the environment and can establish chromatin states which are permissive or repressive to gene expression. Epigenetic regulation of gene expression is cell specific, as such, it is important to understand epigenetic regulation in cells that are thought to play a central role in asthma. As epigenetic processes are critical to cellular specificity and disease susceptibility the overarching hypothesis of this thesis is that alterations to the epigenome of asthmatic airway epithelial cells contribute to the dysregulation of genes involved in key epithelial functions. To investigate this hypothesis, we performed analysis of DNA methylation, expression of epigenetic modifying genes, and histone acetylation and methylation in airway epithelial cells, airway fibroblasts, and peripheral blood mononuclear cells from asthmatic and healthy subjects. We identified unique signatures of both DNA methylation and expression of epigenetic modifying enzymes in airway epithelial cells and showed that epithelial cells were epigenetically distinct from other cell types. Furthermore, we found that airway epithelial cells from asthmatic subjects displayed changes in DNA methylation, expression of histone kinases, acetylation of lysine 18 on histone 3, and occupancy of this histone modification at genes important to epithelial functions. Therefore, epigenetic differences between tissue types were more evident and plentiful than within cell types highlighting the importance of the epigenome to cell specificity, yet subtle differences within each tissue were determined and may play a role in disease pathogenesis. Thus, these findings enhance our understanding of the unique epigenetic landscape which may contribute to the airway epithelial phenotype in health and disease.
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14

McGrogan, Ita. "Release and actions of prostaglandin E¦2 from canine airway epithelium". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0003/NQ42751.pdf.

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15

Amineh, Abbadi. "Hyaluronan Rafts on Airway Epithelial Cells". Cleveland State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=csu1407316041.

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16

Kao, Cheng-Yuan. "Molecular characterization of human airway epithelium innate immunity by IL-17 regulation /". For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2005. http://uclibs.org/PID/11984.

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17

Xenariou, Stefania. "Magnetofection and sonoporation to enhance non-viral gene transfer to airway epithelium". Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433595.

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18

Johnston, Richard A. "Characterization of the airway epithelial bioelectric mechanisms associated with the effects of epithelium-derived relaxing factor in guinea-pig isolated trachea". Morgantown, W. Va. : [West Virginia University Libraries], 2000. http://etd.wvu.edu/templates/showETD.cfm?recnum=1776.

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Thesis (Ph. D.)--West Virginia University, 2000.
Title from document title page. Document formatted into pages; contains ix, 135 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 127-135).
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19

Fischer, Anthony John. "Augmenting antiviral host defense in the respiratory epithelium". Diss., University of Iowa, 2009. https://ir.uiowa.edu/etd/500.

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The airway epithelium has many roles in innate immunity including detection of pathogens and transmitting danger signals to other cell types. However, its role as a primary defender against infection is not well recognized. We have investigated methods of augmenting antiviral immunity by application of agents that stimulate viral killing, either in the extracellular space or within the cytoplasm. A recently described property of airway epithelial cells is direct oxidative killing of bacteria through the coordination of Duox and lactoperoxidase enzymes. We have exploited this property by supplementing airway cells with the lactoperoxidase substrate iodide to prevent viral infection. A second method for enhancing antiviral defenses is to supply small interfering RNAs (siRNAs) targeting essential viral genes. We have optimized antiviral siRNAs targeting respiratory syncytial virus by designing them to specifically target positive sense viral RNAs. Finally, we have initiated a project to discover host defense genes that are expressed in either the submucosal glands surface epithelium of human airway. This information will enable a better characterization of the roles for these structures in host defense pathways, and may identify other targets for augmentation of antiviral immunity.
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20

Ang, Sherlynn. "Characterising and assessing the baseline functionality of the airway epithelium in preterm infants". Thesis, Ang, Sherlynn (2017) Characterising and assessing the baseline functionality of the airway epithelium in preterm infants. Honours thesis, Murdoch University, 2017. https://researchrepository.murdoch.edu.au/id/eprint/39878/.

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Introduction & Aims: Preterm birth rates have risen to over 8% in Australia. The lungs are one of the last organs to develop and therefore, the preterm lung is immature at birth. As effects of premature birth on airway cell function are unknown, we investigated whether preterm nasal epithelial cells (NECs) are inherently different to cells of full-term born infants. Methods: The NECs were obtained via brushing nine preterm born infants (5 males, average gestational age at birth 26.6 ± 2.4 weeks) aged 1.7 years corrected age and nine full-term born infants (5 males) aged 2.3 ± 0.2 years. Submerged monolayer cultures were generated and RNA, protein, supernatant and cytospins were collected. Cell lineage markers were analysed at gene (qPCR) and protein (immunocytochemistry, Western blot) level. Cytokines were measured via ELISA. Two functional assays were performed; wound repair by monolayer culture and transepithelial permeability assay by differentiated, air-liquid interface culture. Results: Preterm NEC were morphologically similar to full-term NEC as monolayer and ALI cultures. Compared to full-term NEC, preterm NECs had significantly higher CK-19 gene expression at passage 1 (1.95 ± 0.51 vs 0.78 ± 0.17; p<0.05) but not CK-5 and vimentin expression. However, CK-19 protein was lower in preterm NECs. Cytokine differences were restricted to higher IL-8 by preterm NECs at passage 3 (31587 ± 3933 vs 15413 ± 5960 pg/mL; p<0.05). Interestingly, transepithelial permeability was significantly lower in preterm children for both particle sizes used (4 kDA: 59.75 vs 324; 20 kDA: 43.26 vs 415.9, p<0.05). Wound repair of preterm NEC was also lower (72 hours: 62.10 vs 100%, p<0.05). Conclusion: Preterm and full-term NECs morphology, gene, protein and cytokine expression were predominantly comparable at baseline. However, interestingly functional differences also existed. Preterm NECs could be used to model mechanisms of preterm respiratory disease.
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21

Relova, Anne-Jacqueline. "Mechanisms for and Effects of Airway Epithelial Damage in Asthma". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2002. http://publications.uu.se/theses/91-554-5312-0/.

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22

Shum, Bennett Oh Vic St Vincent's Clinical School UNSW. "Regulation of allergic asthma by fatty acid-binding proteins". Awarded by:University of New South Wales. St. Vincent's Clinical School, 2007. http://handle.unsw.edu.au/1959.4/27002.

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Fatty acid-binding proteins are small intracellular proteins with poorly defined functions in intracellular fatty acid transport. The adipocyte fatty acid-binding protein aP2 regulates systemic glucose and lipid metabolism. Using Affymetrix microarrays, we found that aP2, in addition to being abundantly expressed by adipocytes, is also expressed by airway epithelial cells. aP2 expression was markedly increased following stimulation of epithelial cells with the Th2 cytokines IL-4 and IL-13, and downregulated by the Th1 cytokine IFN-gamma. Regulation of aP2 mRNA expression by Th2 cytokines was dependent on STAT6, a transcription factor with a major regulatory role in allergic inflammation. We examined aP2 deficient mice in a model of allergic airway inflammation, and found that infiltration of leukocytes, especially eosinophils, into the airways was highly aP2 dependent. T cell priming and peritoneal allergy was unaffected by aP2 deficiency suggesting that aP2 was acting locally within the lung, and analysis of bone marrow chimeras implicated non-haematopoietic cells, most likely airway epithelial cells, as the site of aP2 action in allergic airway inflammation. Expression of the pro-inflammatory cytokines MCP-1 and IL-6 was impaired in cytokine activated aP2 deficient airway epithelial cells, while levels of the anti-inflammatory arachidonic acid metabolite 15-HETE was increased, providing a mechanism for the reduced airway inflammation in aP2 deficient mice. In addition to the immune functions of aP2, we found that the related fatty acid-binding protein mal1 was also upregulated by IL-4/IL-13 in airway epithelial cells, and mal1 deficient mice were protected against airway eosinophilia. Significantly, in comparison to single aP2 deficiency, mice with combined aP2-mal1 deficiency had augmented protection against airway inflammation, and bone marrow chimera experiments demonstrated that aP2-mal1 deficiency affected both non-haematopoeitic and haematopoeitic cells. In T cell priming experiments, aP2-mal1 deficiency resulted in defective cytokine profiles in antigen recall responses, suggesting compromised sensitisation to antigen as one mechanism for aP2-mal1 action in airway inflammation. Together, our data therefore demonstrates the crucial roles of fatty acid-binding proteins in airway epithelium, T cell priming and airway inflammation, and provides a new link between fatty acid signalling and allergy.
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23

Millar, Büchner Pamela [Verfasser], e Marcus A. [Akademischer Betreuer] Mall. "Role of the epithelial Cl- channel SLC26A9 in the murine airway epithelium / Pamela Millar Büchner ; Betreuer: Marcus A. Mall". Heidelberg : Universitätsbibliothek Heidelberg, 2021. http://d-nb.info/1237270790/34.

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24

Farnell, Edward John. "Cloning, disruption and characterisation of Aspergillus fumigatus allergen proteases and their effect on airway epithelial cells". Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/cloning-disruption-and-characterisation-of-aspergillus-fumigatus-allergen-proteases-and-their-effect-on-airway-epithelial-cells(cee1b5be-76cd-477c-bdb8-bdaa945d4e02).html.

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Allergen proteases from a number sources including the filamentous fungus A. fumigatus, are thought to be important in the development of severe asthma through protease dependent interactions with the respiratory epithelium. The first aim of the thesis was to determine the effect of a variety of growth substrates on the secretion of proteases from different strains of A. fumigatus. The second aim was to investigate the effects of recombinant allergen proteases Asp f 5 and Asp f 13 expressed in the P. pastoris protein expression system and crude A. fumigatus culture supernatants on airway epithelial cells and determine whether protease induced interleukin 8 (IL-8) release from airway epithelial cells was dependent on the activation of protease activated receptor 2 (PAR-2).Results demonstrated that the AF293 strain of A. fumigatus secreted serine proteases during growth on pig lung homogenate medium and metalloproteases during growth on a casein based medium but suppressed protease secretion in Vogel's minimal medium. Analysis of the secretion and RNA levels of proteases in A. fumigatus showed that the matrix metalloprotease, Asp f 5 and the serine protease, Asp f 13 were up-regulated and secreted during growth in pig lung medium and that the matrix metalloprotease, Lap1 was up-regulated and secreted along with Asp f 5 and Asp f 13 in casein medium. This finding was confirmed using protease inhibitors and by using strains of A. fumigatus in which Asp f 5 and Asp f 13 genes were disrupted. These results suggest that A. fumigatus was able to detect different complex proteins available as substrates in its environment and regulate protease secretion accordingly. Furthermore, in several strains of A. fumigatus, protease activity was not suppressed by growth in Vogel's medium, suggesting differences in the regulation of protease secretion between strains. Both A. fumigatus culture supernatants and recombinant Asp f 5 and Asp f 13 produced in P. pastoris caused epithelial airway cell desquamination, and IL-8 release in a protease and dose-dependent manner. In addition, both recombinant Asp f 5 and Asp f 13 were both shown to cleave PAR-2 at a site that resulted in receptor activation.In conclusion, differences in the secretion of proteases between A. fumigatus strains and during growth of A. fumigatus on different media suggests a requirement for the standardisation of the preparation of A. fumigatus allergen extracts used both in clinical diagnosis of A. fumigatus allergy and in vitro and in vivo research studies. Furthermore, it is proposed that allergen proteases secreted by A. fumigatus may interact with a variety of host proteins including, matrix molecules, enzymes and receptors which may exacerbate allergic airway diseases.
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25

Leir, Shih-Hsing. "ICAM-1 and CD44 expression in human bronchial epithelium and the role of CD44 isoforms in cell adhesion, migration, and repair". Thesis, University of Southampton, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323933.

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26

Nakatsuka, Yoshinari. "Pulmonary Regnase-1 orchestrates the interplay of epithelium and adaptive immune systems to protect against pneumonia". Kyoto University, 2018. http://hdl.handle.net/2433/235979.

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27

Nordenhäll, Charlotta. "Airway effects of diesel exhaust in healthy and asthmatic subjects". Doctoral thesis, Umeå universitet, Lungmedicin, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-96901.

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Several epidemiological studies have revealed an association between particulate matter (PM) pollution and various health effects. Importantly, there is evidence to suggest that individuals with pre-existing respiratory disease, such as asthma, are more sensitive to elevated ground levels of particulate matter as compared to healthy subjects. Among the various sources of PM pollution, diesel powered vehicles have been identified as important contributors. The aim of this thesis was to investigate the airway effects of experimental chamber exposure to diesel exhaust (DE) in healthy and asthmatic subjects, focusing on airway responsiveness, airway inflammation and lung function. To achieve a comprehensive picture of the airway responses to DE, a number of different methods were used, including lung function measurements, methacholine inhalation tests, induced sputum and bronchoscopy. Each subject acted as his/her own control by being exposed both to filtered air and DE in a crossover design. Short term exposure to DE, at a particle concentration (PMi0) of 300 ug/m3, was associated with a clinically significant increase in bronchial hyperresponsiveness in asthmatic subjects. In accordance with the epidemiological data suggesting a 1-4 day lag effect for most health outcomes to PM pollution, the increase was detected one day after DE exposure, indicating a long lasting response to DE in asthmatic airways. Diesel exhaust induced a range of airway inflammatory changes as reflected in induced sputum, bronchoalveolar lavage and bronchial mucosal biopsies. In healthy subjects, DE exposure was associated with an increase in neutrophils and IL-6 in sputum, elevated levels of IL-8 and IL-6 in bronchial wash (BW), enhanced expression of IL-8 and GRO-a in the bronchial epithelium and with increases in P-selectin and VCAM-1 in the airway mucosa. In contrast, asthmatics responded with an increase in IL-6 in sputum and an enhanced expression of IL-10 in the bronchial epithelium following exposure DE. Thus, clear differences were identified between healthy and asthmatic subjects in the inflammatory response to DE. Airway epithelial cells constitute the first line of cellular defence towards inhaled air pollutants and increasing evidence suggests that these cells contribute markedly to the initiation of airway inflammatory responses. The bronchial epithelium was identified to have an important regulatory role in response to diesel exhaust, including the capacity to produce chemoattractant and immunoregulatory proteins associated with development of airway inflammation and bronchial hyperresponsiveness. Lung function measurements revealed that short-term exposure to DE induces an immediate bronchoconstrictive response in both healthy and asthmatic individuals, with significant increases in airway resistance (Raw) following DE exposure. This thesis also investigated the effects of a lower concentration of DE (PMio 100 ug/m3) than previously studied. It was shown that exposure to DE at a concentration corresponding to a PM level that may be encountered in busy traffic situations, was still associated with potentially adverse airway responses in healthy and asthmatic subjects. In summary, the results presented here indicate that short term exposure to diesel exhaust, at high ambient concentrations, has the potential to induce a range of biological events in the airways of healthy and asthmatic subjects.

Diss. (sammanfattning) Umeå : Umeå universitet, 2002, härtill 4 uppsatser.


digitalisering@umu
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28

Wilson, Kirsty. "Modelling the airway epithelium in vitro as a tool for understanding pulmonary innate defence mechanisms". Thesis, University of Sheffield, 2015. http://etheses.whiterose.ac.uk/13496/.

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Abstract (sommario):
The airway epithelium forms a continuous barrier from the nose to the alveoli and serves a variety of functions. Multiple functionally distinct cell types are involved in these processes. The innate defence functions require a patent airway epithelium, with infections often associated with epithelial defects and phenotypic alterations that are themselves associated with multiple lung diseases. Non-typeable Haemophilus influenzae (NTHi) and respiratory syncytial virus (RSV) are frequently identified in the airways in a range of respiratory diseases These pathogens often trigger exacerbations and worsening symptoms that often result in hospitalisation. This is particularly true in paediatric populations. Although mortality for NTHi and RSV infections alone are themselves low it remains unclear what role these infections play in mortality rates in complex chronic respiratory infections. These studies aimed to establish NTHi and RSV infections within airway epithelium models, and use them as tools to study pulmonary innate defence mechanisms in order to understand the role of these infections in respiratory disease. In vitro airway models were established using lung derived cell lines, undifferentiated primary human bronchial epithelial (uHBE) cells and air-liquid interface (ALI) differentiated uHBE cell cultures. Following establishment of differentiation we validated ALI cultures using a number of markers, including for the putative innate defence PLUNC family proteins, gel-forming mucins and tubulin. These markers are representative of different epithelial cell types within the cultures. Cultures were infected with NTHi or RSV for periods of time ranging from 1 hour to 7 days with a view to establishing chronic infections and allowing biofilm formation. Monolayer cultures showed an enhanced susceptibility to both infections. Cytokine array profiling showed enhanced pro-inflammatory cytokine profiles in response to NTHi and RSV infections in ALI cells resulting in an ability to manage infections compared to monolayer cultures. Expression analysis indicated that both infections altered the transcription of a number of pro-inflammatory genes. Neutrophil products and trypsin were shown to degrade PLUNC proteins in ALI cell secretions. NTHi also appeared to cause degradation of PLUNC proteins suggesting that infection may impair the innate defence shield of the airway epithelium. Our data showed that differential ALI cultures of human airway cells are a useful model for the study of respiratory pathogens.
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29

Yahaya, Badrul H. "Analysis of time-dependent transcriptomic and phenotypic changes associated with repair and regeneration in the airway epithelium". Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4800.

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Abstract (sommario):
The airway epithelium demonstates the ability to quickly repair following physical injury. The morphologic features of this dynamic repair process have been well characterised at the anatomic and cellular level using a number of animal model systems and these studies have provided a solid foundation upon which our understanding of normal repair is build. With the advent of molecular and bioinformatic tools and resources the opportunity exists to extend the value of these models in defining the molecular pathways and interactions that underlay the normal repair process. This thesis represents a realisation of this opportunity. A large animal model was developed in which selected areas of airway epithelium were subjected to bronchial brush biopsy as part of routine bronchoscopic examination prcedures in anaethetised sheep. The process resulted in a physical perturbation of the normal pseudostratified structure of the sheep airwway epithelium at specific locations. By careful experimental design it was possible, within the same animals. to identify and sample from sites undergoing repair at different intervals subsequent in injury. To supplement the histological evaluation of the repair process and align findings with extablished small animal models of airway epithelial repair proliferative cell labelling strategies were implemented in order to study the location and extent of cellular proliferation occurring duringthe repair process. Molecular approaches towards defining the transcriptional response to physical injury comprised application of microarray technology using a commercially sources array platform. Such approach demanted preliminary effort directed towards optimising RNA integrity and yield from airway samples. Following preliminary studies directed towards optimising the model conditions patterns of airway epithelial repair following bronchial brush biopsy were studies in eight sheep at degined time points (6 hours, 1,3, & 7 days) post-injury. Bronchial brush biopsy resulted in the acute removal of the epithelial cell layer and components of the underlying structures. repair processes were rapidly implemented through initial epithelial dedifferentiation, proliferatino and migration at the wound margins and subsequent time-depentend changes in the proportion of subepithelial structures, including smooth muscle and blood vessels, as the epithelial surface moved towards repair. Transcriptional analysis revewaled that over 13,000 probes showed evidence of differential expession at some point during the repair process (p<0.05), whilst of these, 1491 probes had in excess of a two-fold change in expression. array results were validated against conventional semi-quantitative RT-PCR for selected genes. Differentially expressed genes with previously characterised roles in epithelial migration, prolifereation and differentiation were identified during the repair process. The relative emphasis of gene products with particular functional roles varied during the course of repair. Indeed gene ontology (GO) terms identified included those associated with the inflammatory response, cellular migration, extracellular matrix activities, differentiation, proliferation, cellular development, cell cycle activities, cellular adhesion, apoptosis and mitosis. In addition the Kyoto Encyclopedia of Genes and Gneomes (KEGG) databases were queried and such process indicated the involvement of cell communication, 053 and complement and coagulation cascade pathways throughout the repair process, initial (6h) Toll-like receptor and cytokine-cytoine receptor interaction pathways, and the progressive involement of cell cycle, focal adhesion and extracellulaar matrix (ECM)-receptor, and cytokine interaction pathways as the epithelium repaired. The model of airway epithelial injury developed in this thesis generated features broadly consistent with those previosly described in relation to various small animal model systems. Importantly, and in addition, this thesis defines the molecular features associated with repair in this model system and provides a useful resource with which to assess the comparative fetures of the airway transcriptional response to physical injury, It is through such comparison, using analogous methodology, that the fundamental pathways and interactions that underlay normal repair and regeneration can be identified and therafter extended towards inderstanding the basis for variation associated with natural and experimental disease.
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30

Murphy, Desmond Michael. "The potential role of the airway epithelium and novel therapeutic strategies in post-transplant obliterative bronchiolitis". Thesis, University of Newcastle Upon Tyne, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.485564.

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Abstract (sommario):
Long-term survival of lung transplant recipients is limited by development of chronic allograft rejection, manifesting as bronchiolitis obliterans syndrome (BOS), and affecting over 50% of patients surviving more than 5 years post transplant. Unfortunately, current strategies in the management of BOS have had limited impact on its development and progression. The histological lesion of BOS, obliterative bronchiolitis (OB), is characterised by bronchiolar epithelial activation, airway leukocyte infiltration and fibro-proliferation, leading to obliteration of bronchioles through deposition of collagen matrix. The bronchial epithelium is a major source of cytokines, chemokines and growth factors, which contribute to airway inflammation and the airway remodelling process of OB. In this study, I describe the methodology for successful culture of primary bronchial epithelial cells (PBECs) from lung allografts. The establishment of these PBECs has provided a platform to facilitate ex-vivo studies of potential epithelial involvement in the pathophysiology of OB. Using this model, I have shown the ability of IL-I7 (Interleukin-I7), TGF-p (Transforming Growth Factor Beta) and bacterial products to modulate epithelial production of mediators of airway inflammation and remodelling, consistent with the development of OB. Included in my thesis is a pilot study demonstrating that rescue therapy with the macrolide antibiotic, azithromycin resulted in a significant improvement in lung function in patients with BOS. I have also shown through a series of PBEC experiments the potential for azithromycin, simvastatin and phosphodiesterase-4 inhibition to decrease PBEC release of cytokines, chemokines and growth factors critical to airway inflammation and remodelling. The development of a reliable method for the culture of bronchial epithelial cells from lung allografts paves the way for dissecting the involvement of the bronchial epithelium in inflammation, remodelling and fibroproliferation in the transplanted airway. It may also help clarify the role of potential therapeutic agents in the prevention and management of DB in allograft recipients.
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31

Tcacencu, Ion. "Regenerative medicine of the airway cartilage : a morphological and immunohistochemical study with focus on cricoid cartilage defects treated with BMP 2 /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-345-0/.

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32

Ayers, M. "The effect of tobacco smoke on renewal mechanisms in airway epithelium and changes induced by N-acetylcysteine". Thesis, Imperial College London, 1988. http://hdl.handle.net/10044/1/46947.

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33

Tully, Jane Elizabeth. "Classical and alternative nuclear factor-kappaB in epithelium: impacts in allergic airway disease and avenues for redox regulation". ScholarWorks @ UVM, 2014. http://scholarworks.uvm.edu/graddis/500.

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Abstract (sommario):
Nuclear Factor kappaB (NF-êB) is a transcription factor whose activation is increased in settings of allergic asthma. At least two parallel NF-êB pathways exist: the classical pathway, which plays a role in inflammation and cell survival, and the alternative pathway, which regulates lymphoid cell development and organogenesis. The classical NF-êB pathway regulates inflammatory responses derived from lung epithelial cells; however, the role of the alternative pathway in lung epithelial cells remains unclear. We demonstrate that both classical and alternative NF-êB are activated in lung epithelial cells in response to multiple pro-inflammatory agonists, and siRNA-mediated knockdown of alternative NF-êB proteins largely attenuates pro-inflammatory cytokine production. Furthermore, simultaneous activation of both pathways leads to cooperative increases in pro-inflammatory responses, indicating a potential role for both classical and alternative NF-êB in the regulation of epithelial-derived pro-inflammatory responses. NF-êB activation in the epithelium modulates allergic inflammation in mouse models of allergic airway disease, however, its role in the context of an allergen relevant to human asthma remains unknown. In order to address the impact of inhibition of NF-êB in the epithelium in vivo, we utilized a House Dust Mite (HDM)-induced model of allergic airway disease. We demonstrate that HDM exposure activates classical and alternative NF-êB in both murine lung epithelium and human bronchial epithelial cells. Furthermore, following exposure to HDM, airway hyperresponsiveness, neutrophilic inflammation, and remodeling are attenuated in transgenic CC10-NF-êBSR (airway epithelial specific inhibitor of classical and alternative NF-êB) mice in comparison to wild type mice. Our data also demonstrate that specific knockdown of the alternative NF-êB protein, RelB, in the lung partially protects against HDM-induced pro-inflammatory responses, indicating that both classical and alternative NF-êB are important in HDM-induced responses. NF-êB proteins are modified by the redox-dependent post-translational modification, S-glutathionylation, under conditions of oxidative stress. S-glutathionylation of IKKâ, an upstream kinase in the NF-êB pathway, is known to decrease its catalytic activity; however, it is unknown how S-glutathionylation of IKKâ occurs. GSTP is an enzyme that catalyzes protein S-glutathionylation under conditions of oxidative stress and has been associated with the development of allergic asthma. We aimed to determine whether GSTP regulates NF-êB signaling, S-glutathionylation of IKKâ, and pro-inflammatory cytokine production. We demonstrate that siRNA-mediated knockdown of GSTP modulates NF-êB activation, NF-êB transcriptional activity, and pro-inflammatory cytokine production in response to LPS, a component of a bacterial cell wall. Furthermore, we demonstrate that GSTP associates with IKKâ in response to agonist stimulation and dampens IKKâ-induced pro-inflammatory cytokine production, surprisingly, independent of its catalytic activity. We also show that GSTP associates with other proteins of the NF-êB pathway, indicating a potential dual mechanism for repression of NF-êB-induced signaling. These studies collectively demonstrate that classical and alternative NF-êB contribute to epithelial-derived inflammatory responses, and GSTP may be a novel target by which NF-êB can be regulated.
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34

Moisey, Elizabeth Jane. "The innate immune response of large and small airway epithelium to respiratory pathogens in chronic obstructive pulmonary disease". Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3443.

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Abstract (sommario):
Chronic obstructive pulmonary disease (COPD) is a smoking‐related inflammatory lung disease in which small airways remodelling contributes to loss of lung function. Bacterial colonisation in clinically stable COPD patients may play a role in persisting inflammation despite smoking cessation. I propose that the innate immune response from small airway epithelium is more potent than from large airway epithelium, an effect which may be dampened by cigarette smoke, favouring persistent bacterial colonisation in COPD. Nineteen patients with COPD and eleven healthy volunteers were recruited for investigation. Bronchoalveolar lavage (BAL) differential cell counts and cytokine levels were analysed. Standard BAL culture and culture‐independent bacterial DNA analysis were performed. Submerged cultures of epithelial cells from large (LAEC) and small (SAEC) airway were established. Pro‐inflammatory cytokine release in response to cigarette smoke extract (CSE) and non‐typeable Haemophilus influenzae whole cell lysate (HI) was investigated. Increased neutrophil % and cytokine levels (IL‐8, IL‐6, IL‐1β) were detected in COPD BAL samples compared to controls. Culture‐independent microbiological assessment demonstrated bacterial DNA in BAL samples from both COPD patients and controls: the diversity of bacterial species identified was significantly less in COPD samples. Primary airway epithelial cell cultures were successfully established from 16 COPD patients and 10 healthy controls. LAEC and SAEC from COPD patients and controls demonstrated an increase in IL‐8 release in response to combined CSE (5%) and HI. This effect was greater in SAEC, but no significant difference was observed between disease and control cell responses. The same pattern was observed for IL‐6 release. Corticosteroid pre‐treatment (1nM Dexamethasone or 17‐Beclomethasone monopropionate) did not suppress the cellular responses observed. Differences in large and small airway innate immune responses may be important in COPD pathogenesis. This is important to consider in modelling the disease in‐vitro and in the development of new therapeutic targets.
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35

Alonso, Pedro A. "Regional differences in the response of the hamster airway epithelium to elastase: In vivo and In vitro studies". Thesis, Boston University, 1994. https://hdl.handle.net/2144/37997.

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Thesis (Ph.D.)--Boston University
PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
The hamster model of experimental chronic bronchitis comprises a persistent increase in the proportion of bronchial granulated secretory cells after a single intratracheal instillation of elastase. This granulated secretory cell increase, which does not occur in the trachea, has been termed secretory cell metaplasia (SCM). Susceptibility of the bronchial epithelium may be due to a large population of elastase-responsive cells specific to this region. Three dimensional reconstruction of the major form of bronchial secretory cells revealed very little or no rough endoplasmic reticulum (RER), thus demonstrating significant regional heterogeneity since all epithelial secretory cells in the trachea have abundant RER. Animals with bronchial SCM were stimulated with pilocarpine to determine whether the cells subsequent to discharge would re-accumulate granules, thus indicating a permanent phenotypic change. However, bronchial secretory cells failed to discharge at doses equal to and greater than those claimed to be effective in rats. Elastase instilled intratracheally was immuno-localized in the hamster airways to assess the possibility of regional differences in cellular uptake of the enzyme. Elastase was not seen intracellularly in trachea or bronchus suggesting that initiation of bronchial SCM results from a cell surface effect, possibly because of elastase-specific sites on bronchial but not tracheal cells. Tracheal resistance was tested by challenging the epithelial cells in vivo and in vitro with very high doses of elastase. Light and electron microscopy revealed no evidence of a stimulation of the mucus synthetic apparatus, suggesting that tracheal epithelial cells are inherently resistant to proteolytic up-regulation.
2031-01-01
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36

Shao, Xingguo. "Identification of a Tans-differentiation factor, Rad, a small Ras-like GTP-binding protein, in the regulation of epithelial cell differentiation in human airway epithelium /". For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2003. http://uclibs.org/PID/11984.

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37

Acciani, Thomas H. "EGF Receptor Signaling and Diesel Exhaust Particle Exposure in Asthma Pathogenesis". University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1428068959.

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38

Campbell, Sara J. "Mechanisms of Moraxella catarrhalis Induced Immune Signaling in the Pulmonary Epithelium". University of Toledo Health Science Campus / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=mco1268141520.

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39

Bhandari, Anita [Verfasser]. "Impact of cigarette smoke exposure on the airway epithelium of Drosophila melanogaster to model COPD-like phenotypes / Anita Bhandari". Kiel : Universitätsbibliothek Kiel, 2019. http://d-nb.info/1181096731/34.

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40

Perng, Diahn-Warng. "The proinflammatory actions of mast cell tryptase and agonists of protease activated receptor 2 on the human airway epithelium". Thesis, University of Southampton, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327262.

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41

Machala, Anna. "Rhinovirus infection of the human airway epithelium : in vitro characterization of viral replication, inflammatory response, and immunemodulating effects of echinacea". Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/31854.

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Abstract (sommario):
Rhinoviruses (RVs) are the leading cause of upper-respiratory tract infections in humans. To date relatively little is known about the mechanism of RV infection and no cure or prevention exists. Mounting evidence shows that RV replicates very little in its host airway epithelial cells leading researchers to hypothesize that the illness associated with RV infection is the result of the host's immune response, but not necessarily RV replication. This study characterized RV infection in vitro in terms of viral replication, viral RNA, and pro-inflammatory cytokine/chemokine secretion over the course of a typical infection using two distinct airway epithelial cell lines (BEAS-2B and A549) and two different receptor-utilizing RV serotypes (RV14 and RV1A). Cells were infected with known amounts of RV, sampled over 1 week, and assayed for infectious virus, RV14 RNA, and interleukin (IL)-6 and/or IL-8 secretion. For BEAS-2B and A 549 cells viral replication peaked between day 1 (Dl) and D2 post-infection for both RV14 and RV1A, and no significant viral replication was observed after D3. Stimulation of LL-6 and IL-8 was typically not observed before D2 and remained elevated up to D7. Overall, BEAS-2B cells were more susceptible to RV infection than A549, and similar trends were observed for RV14 and RV1A, except RV14 failed to replicate in the A549 cells. Furthermore, UV inactivation of both RV serotypes completely inhibited viral replication and IL-6 secretion in the BEAS-2B model, suggesting the necessity of genetically intact virus to stimulate the IL-6 response. Finally, the effects of two chemically distinct Echinacea extracts on viral replication and IL-6 secretion were investigated in the BEAS-2B model. Neither of the Echinacea extracts had any effect on RV replication, nor did they stimulate IL- 6 secretion in uninfected cells. However, Echinacea treatment of RV infected cells significantly affected IL-6 secretion, but a different trend was observed between RV serotypes, and for the two herb preparations. Overall, RV infection of airway epithelial cells results in relatively low levels of RV replication but a pronounced proinflammatory cytokine/chemokine response which is the likely cause of cold symptoms and a potential target for therapeutics.
Science, Faculty of
Zoology, Department of
Graduate
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42

Larson, Shawnessy Dawn. "The distribution of the neural components within the airway epithelium in healthy animals and animals exposed to allergens and/or ozone /". For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2003. http://uclibs.org/PID/11984.

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43

CARBONE, ANNALUCIA. "Isolation of human amniotic stem cells from term placenta and their in vitro differentation in airway epithelium to correct CF phenotype". Doctoral thesis, Università degli Studi di Cagliari, 2012. http://hdl.handle.net/11584/266062.

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Abstract (sommario):
Cystic fibrosis (CF) is a lethal autosomal recessive disorder due to mutations in the CF transmembrane conductance regulator (CFTR) gene, a cAMP-dependent chloride channel expressed on the apical side of epithelial cells. Although CF involves many organs with secretory/absorptive properties, including the liver, the main cause of morbidity and mortality is a chronic inflammatory lung disease. Because of its monogenic nature, and since the lung is easily accessible, CF has been a target disease for gene-based therapeutic intervention; however, this approach has given unsatisfied results in terms of efficiency of gene delivery to the lung and of efficacy outcomes. This partial success was due to the inefficiency of passing the mucus barrier overlying the epithelial cells and to the immune response against the gene therapy vectors. Cell therapy could be a more effective treatment because allogenic normal cells and autologous engineered cells express CFTR gene. Bone marrow-derived stem cells have been the first source evaluated for homing to the lung and curative potential, but the in vivo efficiency of bone marrow stem cells to differentiate in airways epithelium is very low (0.01–0.025%), as also demonstrated by different studies in CF mice. Recently, new cell sources for CF treatment have been characterized; MSCs from cord blood and amniotic fluid stem cells can differentiate in vitro and in vivo in airway epithelium. Stemming from these results on MSCs, and based on the demonstrated high plasticity of amniotic derived stem cells, after an extensive characterization of the expression of phenotypic and pluripotency markers by hAMSCs and their differentiative potential, we preliminarily evaluated their usefulness in CF by in vitro experiments using cocultures of hAMSCs and CF-respiratory epithelial cells.
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44

Servetnyk, Zhanna. "Functional Aspects of Epithelia in Cystic Fibrosis and Asthma". Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8905.

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The cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP activated chloride channel in the apical membrane of epithelial cells, is defective in patients with cystic fibrosis (CF). Research efforts are focused on chloride channel function in order to find a cure for the disease.

Genistein increased chloride transport in normal and delF508-CFTR cultured airway epithelial cells without cAMP stimulation. Prior pretreatment with phenylbutyrate did not affect the rate of the genistein-stimulated chloride efflux in these cells.

S-nitrosoglutathione is an endogenous bronchodilator, present in decreased amounts in the lungs of CF patients. We studied the effect of GSNO on chloride (Cl-) transport in primary nasal epithelial cells from CF patients homozygous for the delF508-CFTR mutation, as well as in two CF cell lines, using a fluorescent Cl- indicator and X-ray microanalysis. GSNO increased chloride efflux in the CF cell lines and in primary nasal epithelial cells from CF patients. This effect was partly mediated by CFTR. If the cells were exposed to GSNO in the presence of L-cysteine, Cl- transport was enhanced after 5 min, but not after 4 h. GSNO may be a candidate for pharmacological treatment of CF patients.

Chloride transport properties of cultured NCL-SG3 sweat gland cells were investigated. The CFTR protein was neither functional nor expressed in these cells. Ca2+-activated chloride conductance was confirmed and the putative Ca2+-activated chloride channel (CaCC) was further characterized in term of its pharmacological sensitivity.

Corticosteroids, the primary treatment for asthma, cause necrosis/apoptosis of airway epithelial cells. It was investigated whether a newer generation of drugs used in asthma, leukotriene receptor antagonists, had similar effects. Both montelukast and dexamethasone, but not beclomethasone or budesonide induced apoptosis/necrosis in superficial airway epithelial cells. Montelukast and corticosteroids also caused decreased expression of intercellular adhesion molecule -1 (ICAM-1) in epithelial but not endothelial cells.

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45

Pandey, Sumali. "Lung mucosal response to repeated inhalational insults with immunomodulatory agents in a murine model of fungal asthma| Airway epithelium takes the center stage". Thesis, North Dakota State University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3603972.

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Abstract (sommario):

Asthma is a debilitating disease of the lungs affecting 235 million people worldwide. Fungus-associated asthma leads to a particularly severe type of disease, and exposure to environmental fungi and their products is unavoidable due to the ubiquitous nature of fungal species. Besides being allergenic, fungi are opportunistic pathogens, and anti-fungal and/or allergic pathways may be modified through repeated inhalation of immunomodulatory agents, affecting the outcome of fungus-induced asthma.

Our aim in this project was to investigate the extent to which repeated inhalation of immunomodulatory agents influence the lung mucosal responses in a naïve murine host or in one that had been sensitized to fungal proteins (allergic). The immunomodulatory substances chosen hold relevance to human inhalational exposure, and included live or irradiation-killed Aspergillus fumigatus (a fungi) spores, deoxyxnivalenol (a mycotoxin), and fluticasone propionate (an inhalationally administered corticosteroid, commonly prescribed for allergic asthma). In a naïve host, inhalation of live A. fumigatus spores showed pathological features of fungal asthma. However, in an allergen-sensitized lung, both dead and live A. fumigatus spores established fungal airway disease, albeit to different extents. Next, we tested the effect of deoxynivalenol in an allergic host and found that its repeated inhalation did not affect pulmonary disease pathology, but did lead to a dose- and time- dependent increase in mucosal and systemic total IgA. Finally, we tested the effect of fluticasone propionate, and found that it did not influence the development of fungal airway disease, but did induce dynamic changes in lung physiology and antibody titers.

Besides mimicking human inhalational exposures, inhalation ensures direct interaction of the inhaled substances with airway epithelium, which plays an important role in defense against inhaled substances and in asthma pathophysiology. By analyzing various mechanisms involved in murine lung-mucosal response to the inhaled substances, a critical involvement of airway epithelium as an orchestrator of immune responses is highlighted, and this would inform mechanism-based future studies. In conclusion, this project is likely to aid in establishing evidence based standards for fungus-related exposures and in making informed therapeutic decisions for fungus-associated diseases.

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46

Pandey, Sumali. "Lung Mucosal Response to Repeated Inhalational Insults with Immunomodulatory Agents in a Murine Model of Fungal Asthma: Airway Epithelium Takes the Center Stage". Diss., North Dakota State University, 2013. https://hdl.handle.net/10365/26759.

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Abstract (sommario):
Asthma is a debilitating disease of the lungs affecting 235 million people worldwide. Fungus-associated asthma leads to a particularly severe type of disease, and exposure to environmental fungi and their products is unavoidable due to the ubiquitous nature of fungal species. Besides being allergenic, fungi are opportunistic pathogens, and anti-fungal and/or allergic pathways may be modified through repeated inhalation of immunomodulatory agents, affecting the outcome of fungus-induced asthma. Our aim in this project was to investigate the extent to which repeated inhalation of immunomodulatory agents influence the lung mucosal responses in a na?ve murine host or in one that had been sensitized to fungal proteins (allergic). The immunomodulatory substances chosen hold relevance to human inhalational exposure, and included live or irradiation-killed Aspergillus fumigatus (a fungi) spores, deoxyxnivalenol (a mycotoxin), and fluticasone propionate (an inhalationally administered corticosteroid, commonly prescribed for allergic asthma). In a na?ve host, inhalation of live A. fumigatus spores showed pathological features of fungal asthma. However, in an allergen-sensitized lung, both dead and live A. fumigatus spores established fungal airway disease, albeit to different extents. Next, we tested the effect of deoxynivalenol in an allergic host and found that its repeated inhalation did not affect pulmonary disease pathology, but did lead to a dose- and time- dependent increase in mucosal and systemic total IgA. Finally, we tested the effect of fluticasone propionate, and found that it did not influence the development of fungal airway disease, but did induce dynamic changes in lung physiology and antibody titers. Besides mimicking human inhalational exposures, inhalation ensures direct interaction of the inhaled substances with airway epithelium, which plays an important role in defense against inhaled substances and in asthma pathophysiology. By analyzing various mechanisms involved in murine lung-mucosal response to the inhaled substances, a critical involvement of airway epithelium as an orchestrator of immune responses is highlighted, and this would inform mechanism-based future studies. In conclusion, this project is likely to aid in establishing evidence based standards for fungus-related exposures and in making informed therapeutic decisions for fungus-associated diseases.
North Dakota State University. Microbiological Sciences Department
Concordia College (Moorhead, MN). Biology Department
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47

Ruiz, Garcia Sandra. "Appréhender l'hétérogénéité cellulaire et la dynamique de différenciation des épithéliums des voies aériennes au moyen de signatures transcriptionnelles sur cellule unique". Thesis, Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4204/document.

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Les voies aériennes humaines sont bordées d'un épithélium pseudostratifié composé principalement de cellules basales et de cellules pyramidales parmi lesquelles figurent les cellules sécrétrices de mucus et les cellules multiciliées. Toutes ces cellules contribuent à la clairance mucociliaire des voies respiratoires. Cet épithélium se régénère lentement dans des conditions homéostatiques, mais il est capable de se régénérer rapidement après agression grâce à des processus de prolifération, de migration, de polarisation et de différenciation. Chez les patients atteints de maladies respiratoires chroniques telles que la broncho-pneumopathie chronique obstructive, l'asthme ou la mucoviscidose, la réparation tissulaire est souvent défectueuse, caractérisée par une perte de cellules multiciliées et une hyperplasie des cellules sécrétrices, ayant pour conséquence une clairance mucociliaire affectée. La séquence des événements cellulaires conduisant à un tissu fonctionnel ou remodelé est encore mal décrite. Notre principal objectif a été d’identifier les types cellulaires successifs mis en jeu lors de la régénération tissulaire et les événements moléculaires responsables d'une régénération saine ou pathologique. Nous avons analysé la composition cellulaire de l’épithélium des voies respiratoires à plusieurs stades de différenciation en utilisant un modèle de culture 3D in vitro qui reproduit la composition cellulaire in vivo. En appliquant une méthode de transcriptomique sur cellule unique couplée à des méthodes bioinformatiques, nous avons établi les hiérarchies cellulaires permettant de reconstruire les différentes trajectoires cellulaires mises en jeu lors de la régénération de l’épithélium des voies respiratoires humaines. Après avoir confirmé les lignages cellulaires qui ont été précédemment décrits, nous avons découvert une nouvelle trajectoire reliant les cellules sécrétrices de mucus aux cellules multiciliées. Nous avons également caractérisé de nouvelles populations cellulaires et de nouveaux acteurs moléculaires impliqués dans le processus de régénération de l'épithélium des voies respiratoires humaines. Enfin, grâce à ces approches, nous avons mis en évidence des réponses spécifiques de chaque type cellulaire survenant dans des situations pathologiques d’hyperplasie sécrétoire. Ainsi, nos données, en apportant d'importantes contributions à la compréhension de la dynamique de différenciation de l’épithélium des voies respiratoires humaines, ouvrent de nouvelles voies vers l’identification de cibles thérapeutiques
Human airways are lined by a pseudostratified epithelium mainly composed of basal and columnar cells, among these cells we can find multiciliated, secretory cells and goblet cells. All these cells work together in the mucociliary clearance of the airways. This epithelium regenerates slowly under homeostatic conditions but is able to recover quickly after aggressions through proliferation, migration, polarization and differentiation processes. However, in patients with chronic pulmonary diseases such as chronic obstructive pulmonary disease, asthma or cystic fibrosis, epithelial repair is defective, tissue remodeling occurs, leading to loss of multiciliated cells and goblet cell hyperplasia, impairing correct mucociliary clearance. The sequence of cellular events leading to a functional or remodelled tissue are still poorly described. Hence, we aim at identifying the successive cell types appearing during tissue regeneration and the molecular events that are responsible for healthy or pathological regeneration. We have analysed airway epithelial cell composition at several stages of differentiation using an in vitro 3D culture model which reproduces in vivo epithelial cell composition. Applying single cell transcriptomics and computational methods, we have identified cell lineage hierarchies and thus constructed a comprehensive cell trajectory roadmap in human airways. We have confirmed the cell lineages that have been previously described and have discovered a novel trajectory linking goblet cells to multiciliated cells. We have also discovered novel cell populations and molecular interactors involved in the process of healthy human airway epithelium regeneration. Using these approaches, we have finally shed light on cell-type specific responses involved in pathological goblet cell hyperplasia. Our data, by bringing significant contributions to the understanding of differentiation’s dynamics in the context of healthy and pathological human airway epithelium, may lead to the identification of novel therapeutic targets
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48

Österlund, Camilla. "Activation of lung epithelial cells by group 2 mite allergens". Doctoral thesis, Umeå universitet, Lungmedicin, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-51619.

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Abstract (sommario):
Throughout many parts of the world house dust mites (HDM) are considered as a major source of indoor aeroallergens and they are powerful inducers of allergic diseases. Proteolytic HDM allergens are recognised as being able to directly activate respiratory epithelial cells and thereby actively participate in innate immune responses. Although several major HDM allergens lack proteolytic activity, their possible ability to similarly interact with epithelial cells is not known. The overall aim of this thesis was therefore to elucidate if and how major non-proteolytic group 2 allergens from different mite species interact with respiratory epithelial cells. The effects of the structurally related Der p 2, Der f 2 and Eur m 2 from different HDM species as well as the storage mite allergen Lep d 2 were studied in vitro using human respiratory epithelial cells. Also the non-proteolytic, but structurally dissimilar, Fel d 1 from cat, Can f 2 from dog, Bet v 1 from birch and Phl p 5a from timothy were studied. In this thesis evidence that major group 2 mite allergens activate bronchial epithelial cells is presented. Following allergen exposure the secreted amount of the inflammatory mediators G-CSF, GM-CSF, IL-6, IL-8, MCP-1, MIP-3α and sICAM-1 was increased. Surface expression of ICAM-1 was also increased following allergen exposure. Moreover, Fel d 1 and Can f 2 induced secretion of the same mediators from bronchial epithelial cells, representing two additional protein structures being able to directly induce cell activation. In experiments using specific inhibitors and siRNA transfection, it was shown that the mite allergens engage TLR4 and activation through MyD88, MAPK and NF-κB signal transduction pathways. In conclusion, the novel findings in this thesis provide knowledge on how major aeroallergens, in addition to their ability to provoke specific adaptive immune responses, may aggravate a respiratory airway disease by adjuvant-like activation of inflammatory responses in bronchial epithelial cells. This differs from previously reported allergen-induction of epithelial cells by the clear independency of proteolytic activation.
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49

Steiert, Sabrina [Verfasser], Carsten [Akademischer Betreuer] Schmidt-Weber e Klaus [Akademischer Betreuer] Schümann. "Evaluation of Anti-inflammatory Potential of Tesalin on Airway Epithelium and Innate Immune Effector Cells / Sabrina Steiert. Betreuer: Carsten Schmidt-Weber. Gutachter: Carsten Schmidt-Weber ; Klaus Schümann". München : Universitätsbibliothek der TU München, 2016. http://d-nb.info/1091562113/34.

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50

Ruiz, Garcia Sandra. "Appréhender l'hétérogénéité cellulaire et la dynamique de différenciation des épithéliums des voies aériennes au moyen de signatures transcriptionnelles sur cellule unique". Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4204.

Testo completo
Abstract (sommario):
Les voies aériennes humaines sont bordées d'un épithélium pseudostratifié composé principalement de cellules basales et de cellules pyramidales parmi lesquelles figurent les cellules sécrétrices de mucus et les cellules multiciliées. Toutes ces cellules contribuent à la clairance mucociliaire des voies respiratoires. Cet épithélium se régénère lentement dans des conditions homéostatiques, mais il est capable de se régénérer rapidement après agression grâce à des processus de prolifération, de migration, de polarisation et de différenciation. Chez les patients atteints de maladies respiratoires chroniques telles que la broncho-pneumopathie chronique obstructive, l'asthme ou la mucoviscidose, la réparation tissulaire est souvent défectueuse, caractérisée par une perte de cellules multiciliées et une hyperplasie des cellules sécrétrices, ayant pour conséquence une clairance mucociliaire affectée. La séquence des événements cellulaires conduisant à un tissu fonctionnel ou remodelé est encore mal décrite. Notre principal objectif a été d’identifier les types cellulaires successifs mis en jeu lors de la régénération tissulaire et les événements moléculaires responsables d'une régénération saine ou pathologique. Nous avons analysé la composition cellulaire de l’épithélium des voies respiratoires à plusieurs stades de différenciation en utilisant un modèle de culture 3D in vitro qui reproduit la composition cellulaire in vivo. En appliquant une méthode de transcriptomique sur cellule unique couplée à des méthodes bioinformatiques, nous avons établi les hiérarchies cellulaires permettant de reconstruire les différentes trajectoires cellulaires mises en jeu lors de la régénération de l’épithélium des voies respiratoires humaines. Après avoir confirmé les lignages cellulaires qui ont été précédemment décrits, nous avons découvert une nouvelle trajectoire reliant les cellules sécrétrices de mucus aux cellules multiciliées. Nous avons également caractérisé de nouvelles populations cellulaires et de nouveaux acteurs moléculaires impliqués dans le processus de régénération de l'épithélium des voies respiratoires humaines. Enfin, grâce à ces approches, nous avons mis en évidence des réponses spécifiques de chaque type cellulaire survenant dans des situations pathologiques d’hyperplasie sécrétoire. Ainsi, nos données, en apportant d'importantes contributions à la compréhension de la dynamique de différenciation de l’épithélium des voies respiratoires humaines, ouvrent de nouvelles voies vers l’identification de cibles thérapeutiques
Human airways are lined by a pseudostratified epithelium mainly composed of basal and columnar cells, among these cells we can find multiciliated, secretory cells and goblet cells. All these cells work together in the mucociliary clearance of the airways. This epithelium regenerates slowly under homeostatic conditions but is able to recover quickly after aggressions through proliferation, migration, polarization and differentiation processes. However, in patients with chronic pulmonary diseases such as chronic obstructive pulmonary disease, asthma or cystic fibrosis, epithelial repair is defective, tissue remodeling occurs, leading to loss of multiciliated cells and goblet cell hyperplasia, impairing correct mucociliary clearance. The sequence of cellular events leading to a functional or remodelled tissue are still poorly described. Hence, we aim at identifying the successive cell types appearing during tissue regeneration and the molecular events that are responsible for healthy or pathological regeneration. We have analysed airway epithelial cell composition at several stages of differentiation using an in vitro 3D culture model which reproduces in vivo epithelial cell composition. Applying single cell transcriptomics and computational methods, we have identified cell lineage hierarchies and thus constructed a comprehensive cell trajectory roadmap in human airways. We have confirmed the cell lineages that have been previously described and have discovered a novel trajectory linking goblet cells to multiciliated cells. We have also discovered novel cell populations and molecular interactors involved in the process of healthy human airway epithelium regeneration. Using these approaches, we have finally shed light on cell-type specific responses involved in pathological goblet cell hyperplasia. Our data, by bringing significant contributions to the understanding of differentiation’s dynamics in the context of healthy and pathological human airway epithelium, may lead to the identification of novel therapeutic targets
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