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Relevant bibliographies by topics / Airway inflammation / Dissertations / Theses

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Dissertations / Theses on the topic 'Airway inflammation'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Zhao, Jingyue. "Th17 responses in airway inflammation and airway remodelling." Thesis, King's College London (University of London), 2011. http://kclpure.kcl.ac.uk/portal/en/theses/th17-responses-in-airway-inflammation-and-airway-remodelling(94ca2e63-6304-4694-998e-b40747ca0f9a).html.

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2

Liu, Jia Clinical School Prince of Wales Hospital Faculty of Medicine UNSW. "Nitric oxide in airway inflammation." Publisher:University of New South Wales. Clinical School - Prince of Wales Hospital, 2009. http://handle.unsw.edu.au/1959.4/43678.

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Exhaled breath condensate (EBC) is a non-invasive method of investigating airway inflammation associated with nitric oxide (NO) and the metabolites nitrite/nitrates (NOx) in diseases such as chronic obstructive pulmonary disease (COPD), but some of the variables affecting the results are unknown. It was hypothesised that 1) EBC would be influenced by lung volumes and the type of EBC collection device; 2) fractional exhaled NO (FENO) and EBC NOx in COPD patients would be altered by smoking and glucocorticosteroids (GCS); 3) cigarette smoke could contribute to the EBC NOx concentration while it

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3

Mulrennan, Siobhain A. "Diagnosis and treatment in airway inflammation." Thesis, University of Hull, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441682.

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4

Siva, Roshan. "Modulation of airway inflammation in COPD." Thesis, University of Leicester, 2006. http://hdl.handle.net/2381/4732.

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Inflammation in foregut derivatives outside the lung may contribute to amplification of airway inflammation. I have shown that a management strategy aiming to minimise eosinophilic airway inflammation as well as symptoms is associated with a significant 62% reduction in the frequency of severe exacerbations of COPD. This strategy was associated with no overall increase in corticosteroid treatment; there was evidence that increased corticosteroid therapy was targeted to patients with eosinophilic airway inflammation and benefit was largely confined to these patients. I have shown an association

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5

Kölbeck, Karl-Gustav. "Nasal and bronchial airway reactivity in allergic and non allergic airway inflammation /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-428-3/.

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6

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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7

Kelly, M. G. "Air way inflammation in obstructive airway diseases." Thesis, Queen's University Belfast, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273059.

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8

Ratnawati, Ratnawati Prince of Wale Hospital Clinical School UNSW. "Exhaled nitric oxide in asthmatic airway inflammation." Awarded by:University of New South Wales. Prince of Wale Hospital Clinical School, 2006. http://handle.unsw.edu.au/1959.4/25729.

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Measuring the level of exhaled NO (eNO) in the breath is a new method to monitor airway inflammation in asthma and may have a role in the management of asthma. The hypotheses were that eNO will reflect the degree of inflammation in chronic asthma, and will indicate how anti- inflammatory therapy should be altered to improve asthma control. Three studies were performed to test the hypotheses. A cross sectional study was performed to define the normal range of eNO and to compare this range with those who have asthma or atopy. The second study was observational, to compare the level of eNO during

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9

Gauvreau, Gail M. "Pharmacological modulation of allergen-induced airway inflammation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0001/NQ42847.pdf.

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10

Jatakanon, Anon. "Noninvasive assessment of airway inflammation in asthma." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312719.

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11

Hilliard, Thomas Norman. "Airway inflammation and remodelling in cystic fibrosis." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427686.

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12

Montefort, Stephen. "Cell adhesion in airway mucosal allergic inflammation." Thesis, University of Southampton, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240611.

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13

Ip, Sau-man Mary. "A pathophysiologic study of airway inflammation in bronchiectasis." [Hong Kong : University of Hong Kong], 1991. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13793895.

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14

Zheng, Ling 1958. "Airway inflammation and remodelling post human lung transplantation." Monash University, Dept. of Medicine, 2002. http://arrow.monash.edu.au/hdl/1959.1/8099.

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15

Dahlin, Joakim. "Mast Cell Progenitor Trafficking in Allergic Airway Inflammation." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-206608.

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Mast cell progenitors originate from the bone marrow and migrate to the lungs via the blood. During maturation, these cells acquire granules that contain a potent array of bronchoconstrictive mediators. The number of pulmonary mast cells is augmented in asthmatic patients and in mice with allergic airway inflammation, possibly contributing to airway hyperreactivity. An increase in mast cells is likely due to an increased recruitment of committed mast cell progenitors from the blood. However, until now a committed mast cell progenitor population has not been found in adult peripheral blood. We

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16

Blair, Alan. "Role of bradykinin in virus-induced airway inflammation." Thesis, Cardiff University, 2009. http://orca.cf.ac.uk/54363/.

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Asthma is a chronic inflammatory disease of the airways and viral infections account for the majority of exacerbations and may play a role in its pathogenesis. Bradykinin levels are increased in the lungs of asthmatics and inhaled bradykinin produces bronchoconstriction in asthmatic but not in normal patients. In this study, guinea-pigs were inoculated with parainfluenza and influenza virus to establish airways inflammation and hyperreactivity. The role of bradykinin in the parainfluenza model was examined by using the tissue kallikrein inhibitor, FE999024, and the bradykinin B2 receptor antag

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17

葉秀文 and Sau-man Mary Ip. "A pathophysiologic study of airway inflammation in bronchiectasis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1991. http://hub.hku.hk/bib/B31981434.

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18

McKay, Anne. "The role of immune mediators in airway inflammation." Thesis, University of Glasgow, 2004. http://theses.gla.ac.uk/4828/.

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Asthma is a chronic inflammatory condition of the airways characterised by reversible airflow obstruction, airway hyper-responsiveness and inflammatory infiltrates in the airway walls containing eosinophils, T lymphocytes and mast cells. T helper (Th) lymphocyte subsets, defined by the cytokines they secrete, are thought to play a key role in the in the initiation and perpetuation of chronic airway inflammation. Th2 cells, producing interleukin (IL)-4, IL-5, IL-9 and IL-13, are thought to be of particular importance. In contrast, Thl cells producing interferon (IFN)-y may counteract the develo

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19

Fitch, Patrick Stephen. "A study of airway inflammation in childhood asthma." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326411.

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20

Pereira, Ana Marta Pinheiro. "Is competitive swimming associated with increased airway inflammation?" Master's thesis, Faculdade de Medicina da Universidade do Porto, 2009. http://hdl.handle.net/10216/50162.

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21

Correia, De Paiva Claudia. "The control of inflammation in airway epithelial cells." Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/16785/.

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COPD is a severe chronic and complex airway disease that represents a major financial burden on the healthcare and economic system. Environmental risk factors such as cigarette smoke have been associated with the predisposition to COPD. Other factors such as exposure to viral pathogens can exacerbate airway inflammation and tissue destruction generated by recruited neutrophils, culminating in altered epithelial cell responses in COPD. This thesis investigated the physiological role of Pellino-1, an E3-ubiquitin ligase, and its regulation in human primary bronchial epithelial cells (HBEpCs) in

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22

Gupta, Vandana. "Pharmacological targeting of neutrophilic airway inflammation in COPD." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/pharmacological-targeting-of-neutrophilic-airway-inflammation-in-copd(73df122b-f031-445e-a6a9-bbcc0039b6c6).html.

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Background: COPD is characterised by increased neutrophilic inflammation which further increases during exacerbations. Corticosteroids are currently one of the mainstays of treatment but they have limited effectiveness; there is a great need to develop new anti-inflammatory pharmacotherapies for use in COPD. Inhaled LPS has been used as a model of increased neutrophilic inflammation in healthy patients, smokers and asthmatics. Its use in patients with COPD as a model of exacerbations has not yet been evaluated. PI3 kinase is a vital intracellular enzyme, which upon activation leads to a number

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23

Pereira, Ana Marta Pinheiro. "Is competitive swimming associated with increased airway inflammation?" Dissertação, Faculdade de Medicina da Universidade do Porto, 2009. http://hdl.handle.net/10216/50162.

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24

Wood, Lorna J. "The role of bone marrow progenitor cells in allergen-induced airway hyperresponsiveness and airway inflammation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0028/NQ51023.pdf.

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25

Laing, Ingrid A. "Candidate gene approach to investigating airway inflammation and asthma." University of Western Australia. School of Paediatrics and Child Health, 2005. http://theses.library.uwa.edu.au/adt-WU2005.0097.

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[Truncated abstract] Asthma genetic studies have identified many genes that contribute to the pathogenesis of asthma and related variables. Members of the secretoglobin family appear to play an important role in controlling airway inflammation but they have received relatively little attention in asthma genetic research. In this thesis, I have investigated the genes of two members of the secretoglobin family (16 kDa Clara cell secretory protein (CC16) and secretoglobin 3A2 (SCGB3A2)) that are expressed at high levels in the airways and are important anti-inflammatory agents. The overall aim of

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26

Gajewska, Beata Urszula Jordana Manel. "Generation of immune responses in experimental allergic airway inflammation /." [Hamilton, Ont.] : McMaster University, 2004.

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27

Laing, Ingrid A. "Candidate gene approach to investigating airway inflammation and asthma /." Connect to this title, 2004. http://theses.library.uwa.edu.au/adt-WU2005.0097.

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28

Clarke, Deborah Lee. "The role of prostanoids and isoprostanes in airway inflammation." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406342.

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29

Hamilton, Lynnsey M. "Tyrosine kinase dependent mechanisms underlying airway inflammation in asthma." Thesis, University of Southampton, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.423571.

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30

Mirchandani, Ananda. "IL-33-induced innate lymphoid cells and airway inflammation." Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/4527/.

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31

Koombua, Kittisak. "Multiscale Modeling of Airway Inflammation Induced by Mechanical Ventilation." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1841.

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Mechanical ventilation (MV) is a system that partially or fully assists patients whose respiratory system fails to achieve a gas exchange function. However, MV can cause a ventilator-associated lung injury (VALI) or even contribute to a multiple organ dysfunction syndrome (MODS) in acute respiratory distress syndrome (ARDS) patients. Despite advances in today technologies, mortality rates for ARDS patient are still high. A better understanding of the interactions between airflow from mechanical ventilator and the airway could provide useful information used to develop a better strategy to vent

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32

Kharitonov, Sergei Alexandrovich. "Exhaled nitric oxide in airway diseases." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266411.

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33

Barker, Bethan Louise. "Exploring the interplay between airway bacteria, airway inflammation, lung structure and skeletal muscle dysfunction in COPD." Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/39977.

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Airway bacteria, airway inflammation, lung structure and skeletal muscle dysfunction are all recognised as important components of chronic obstructive pulmonary disease (COPD), yet the interplay between these components is not well understood. Within this thesis I present an observational study exploring relationships between airway inflammation and molecular measures of potentially pathogenic bacteria. I have shown that airway bacterial detection is associated with increased airway inflammation in stable COPD, and that this association appears to be driven by Haemophilus influenzae. I then pr

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34

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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35

Jonasson, Sofia. "Lung mechanics and airway inflammation in murine models of asthma." Doctoral thesis, Uppsala universitet, Klinisk fysiologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-107061.

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Allergic asthma is an inflammatory disease of the airways and is characterized by eosinophilic inflammation and increased airway reactivity. In the studies presented in this thesis, lung mechanics and measurements of airway reactivity were assessed in anaesthetized tracheostomized mice by using an animal ventilator (flexiVent®). A forced oscillation technique makes it possible to measure of both airway and tissue mechanics with a potential to distinguish between central and peripheral airways. The results of the experiments on lung mechanics imply that it is important to understand how altered

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36

Noble, Donald D. "Biophysical, biochemical and cellular markers of airway inflammation in asthma." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/25029.

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Respiratory heat and moisture loss (RHML) is proposed as a novel biophysical marker of AI. In a cross-sectional study of 23 patients with stable persistent asthma, 19 patients with acute asthma and 18 controls, RHML was significantly elevated in stable asthma (p=<0.01) and correlated with sputum eosinophil percentage (r=0.73; p=<0.01). Paradoxically, RHML was not elevated in acute asthma, and a number of possible explanations are discussed. The exhaled gases nitric oxide (NO) and carbon monoxide (CO), and exhaled breath condensate (EBC) pH and nitrite were examined in a cross-sectional s

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37

Farhadi, Nazanin. "The role of Natural Killer cells in allergic airway inflammation." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/38444.

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Natural Killer (NK) cells are innate cells of the immune system and constitute 10% of lung lymphocytes. Increasing evidence implicates a role for innate immunity in the pathogenesis of asthma and although there is evidence of a role for NK cells in the development of allergic inflammation, the mechanisms by which NK cells contribute to allergy is not known. To characterise the NK cell response and determine the phenotype of NK cells in allergic pulmonary inflammation we employed a model in which mice are dosed intranasally 3 times a week for 3 weeks with house dust mite (HDM) extract. Numbers

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38

Bosson, Jenny. "Ozone and diesel exhaust : airway signaling, inflammation and pollutant interactions." Doctoral thesis, Umeå : Univ, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1071.

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39

Müller, Malin. "Apoptosis in chronic inflammation, with specific reference to airway disease /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-925-4/.

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40

Palm, Jörgen. "Nasal airway nitric oxide : methodological aspects and influence of inflammation /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-801-7/.

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41

McCluskie, Kerryn. "Pharmacological modulation of an 'in vivo' model of airway inflammation." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.415013.

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42

Brims, Fraser John Hall. "Airway procoagulant activity and inflammation in moderate and severe asthma." Thesis, University of Nottingham, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496732.

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Asthma is a chronic disease characterised by airway inflammation and remodelling. Inhaled corticosteroids (ICS) are the cornerstone of asthma therapy, and yet many asthmatics remain symptomatic, some with severe manifestations of the disease. The bronchial epithelium produces coagulation factors locally in the absence of plasma exudation. There is evidence in asthma that there is upregulation and stimulation of the external coagulation cascade in the airways, and locally derived factors may be involved.

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43

Ketchell, Robert Ian. "Pharmacological modulation of mast cell-mediated airway inflammation in asthma." Thesis, King's College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408913.

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44

Thursfield, Rebecca Marie. "Infection, inflammation & innate immunity in the paediatric CF airway." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/43757.

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This thesis focuses on infection and immunity within the airways in cystic fibrosis (CF), particularly the role of the antimicrobial peptides (part of the innate immune system) and their relationship to vitamin D status. Vitamin D response elements have been identified in the genes encoding the antimicrobial peptides cathelicidin (LL37) and human β defensins (HBD-2) and in-vitro vitamin D significantly induces expression of these peptides in both CF and non-CF bronchial epithelial cells. As innate defence is pivotal to airway health and is one of the proposed ways that vitamin D deficiency con

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45

Reader, Brenda Faye. "Social Stress Induces Immunoenhancement During Allergic Airway Inflammation and Infection." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1385475903.

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46

Murphy, Grace E. J. "IL-33 and ST2 in innate and adaptive airway inflammation." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6685/.

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Background: ST2 has been identified in playing an important role in Th2-mediated inflammation and asthma. IL-33 acts as the ligand for ST2; it is a novel cytokine that induces innate Th2/type-2 responses when delivered to the lung. The hierarchy of IL-33 and type-2 cytokines and chemokines in Th2 inflammation in the lung has not been fully elucidated. Furthermore, the role of IL-33 in the adaptive response in allergic mediated airways disease is unclear. Epithelial cells (ECs) are increasingly recognised as having an immunological role in airway inflammation and asthma, in particular releasing

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47

Swaidani, Shadi. "THE ROLE OF ACT1 IN IL-25 DEPENDENT TH2 RESPONSES AND ALLERGIC AIRWAY INFLAMMATION AND AIRWAY HYPERRESPONSIVENESS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1270240862.

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48

Hagner, Matthias [Verfasser], and Ana [Akademischer Betreuer] Martin-Villalba. "Relationship between impaired mucociliary clearance and airway inflammation in chronic airway diseases / Matthias Hagner ; Betreuer: Ana Martin-Villalba." Heidelberg : Universitätsbibliothek Heidelberg, 2017. http://d-nb.info/1177688743/34.

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49

Gupta, Sumit. "Scanning the asthmatic airway : defining relationship between physiology, inflammation and airway structure in severe asthma using computed tomography." Thesis, University of Leicester, 2012. http://hdl.handle.net/2381/27589.

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Severe asthma is a complex and heterogeneous disease characterised by chronic airway inflammation, disordered airway physiology and airway remodelling. Computed tomography (CT) has emerged as a non-invasive tool for assessment of airway structural changes. A critical gap in our understanding of severe asthma is the ability to relate structural changes to important clinical outcomes. This thesis examines the relationship between CT assessed airway structure, airway inflammation and airway physiology in severe asthma patients. I first present the largest qualitative study of CT findings in sever

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50

Lensmar, Catarina. "Early airway inflammation in allergic asthma : aspects of pulmonary innate immunity /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4463-6/.

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