Dissertations / Theses on the topic 'Airway inflammation'
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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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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 may also decrease FENO indirectly by converting airway NO to NOx. It was found that EBC volume was significantly correlated with both tidal volume and minute volume. Comparing four EBC collection devices demonstrated greater efficiency with the ECoScreen?? than siliconised glass tubes or RTube?? but it gave factitiously high NOx levels. Total EBC protein levels over a 10-minute collection were significantly higher using the ECoScreen?? than either glass or RTube?? devices. A cross-sectional study of 96 COPD patients and 80 age-matched control subjects demonstrated that FENO levels in COPD patients were significantly higher than normal subjects when comparing either the combined groups or appropriate two subgroups: ex-smokers and smokers. GCS treatment demonstrated no significant effect on either FENO levels or EBC NOx, but EBC NOx was elevated in smokers. In vitro, cigarette smoke extract (CSE) induced significantly higher NOx and asymmetric dimethylarginine (ADMA) levels in A549 cells when compared with control media. The anti-oxidant, NAC pre-treatment partially reversed the elevated NOx levels but not the ADMA levels. This thesis is the first to report FENO and EBC NOx in COPD patients in an appropriate sample size to be able to evaluate each subgroup, and the increased EBC NOx levels found in smokers in vivo was consistent with the elevated NOx level in response to CSE observed in vitro. These data indicate that smoking-related airway inflammation and activation of the NO pathway are complex with both an increase in ADMA, NO, NOx and may be regulated by oxidative stress rather than the nitric oxide synthase (NOS) pathway.
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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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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 between the sputum differential neutrophil count and airway bacterial load, and showed that a one week course of Levofloxacin significantly reduced both the % neutrophil count and bacterial load in patients with stable state COPD and bacterial load > 106 cfu/ml. I have shown that the prevalence of peptic ulcer disease increases progressively with increasing severity of COPD in miners with homogeneous risk factors for development of COPD, and that peptic ulceration was a strong and independent predictor of a low FEV1 % predicted and FEV1/FVC ratio. In another population I showed that H.Pylori seropositivity was more common in patients with COPD compared to healthy smokers matched for age and occupation.;We have shown that TREM-1 can be measured from induced sputum and is potentially a novel marker of bacterial infection and neutrophilic airway inflammation during exacerbations.;Further work is required to ensure that measurement and modulation of airway inflammation results in improved clinical outcomes, and is made more clinically viable.
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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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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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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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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 and after an exacerbation of asthma. The third study was an interventional study to evaluate eNO in management of paediatric asthma. In this latter study the level of eNO was measured to monitor airway inflammation in asthmatic children with the intention of adjusting antiinflammatory drugs (inhaled glucocorticosteroids) according to the level of eNO. These studies have shown that the mean level of eNO was significantly higher in asthmatic compared with normal subjects, but not significantly different when compared with atopic non-asthmatic subjects. eNO was correlated with the number of positive skin prick tests in atopic subjects whether asthmatic or nonasthmatic. The eNO level was increased during acute exacerbations of asthma and decreased after two weeks with therapy of GCS. In a pilot study eNO appeared to be superior to FEV1 in adjusting the dose of iGCS to control asthmatic children, but this needs to be confirmed with a larger sample size. Another non-invasive method to detect inflammatory markers is the technique of exhaled breath condensate (EBC). Although NO is degraded to NOx, it was found that eNO had no significant correlation with EBC NOx but had a significant correlation with pH. Hypertonic saline challenge, an artificial model of an asthmatic exacerbation was associated with an increase in EBC volume and the release of histamine, implicating mast cell activation. These novel findings suggest that non-invasive markers can be used both for clinical and mechanistic proposes.
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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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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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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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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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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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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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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 isolated Lin- c-kithi ST2+ integrin β7hi CD16/32hi progenitors from murine blood and showed that these cells were committed to the mast cell lineage. Based on the expression of FcεRI, these cells were less mature in Th1-prone C57BL/6 mice than in Th2-prone BALB/c mice. Asthma is associated with elevated levels of IgE. Upon exposure to allergens, IgE immune complexes are formed. In a mouse model of allergic airway inflammation, we showed that intranasal administration of IgE immune complexes to antigen-sensitized mice resulted in an increased number of mast cell progenitors compared with antigen administration alone. The increase in mast cell progenitors was independent of the low-affinity IgE receptor CD23. Rather, signaling through the common FcRγ-chain was required to enhance the number of lung mast cell progenitors. Signaling through FcεRI was likely responsible for the increase. However a role for FcγRIV could not be excluded. CD11c+ cells, such as dendritic cells, are important for antigen sensitization. In a mouse model of allergic airway inflammation, these cells are also important for the development of airway hyperreactivity, eosinophilia and Th2 cytokine production in response to antigen challenge. We showed that CD11c+ cells are critical for the recruitment of lung mast cell progenitors and the subsequent increase in mast cells. These CD11c+ cells were needed for the upregulation of endothelial vascular cell adhesion molecule-1 (VCAM-1), which is a prerequisite for the antigen-induced recruitment of lung mast cell progenitors.
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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 antagonist, MEN16132. Firstly, the effects of bradykinin inhalation in conscious guinea-pigs were characterized by using inhibitors of its breakdown and selective antagonists. Inhaled bradykinin produced a bronchoconstriction only after treatment with the inhibitors of angiotensin converting enzyme and/or neutral endopeptidase, captopril and phosphoramidon respectively. Inhaled bradykinin also increased inflammatory cell influx to the lungs when its breakdown was inhibited with both drugs. Cell influx and bronchoconstriction were blocked by the B2 receptor antagonists icatibant and MEN16132. These responses were therefore B2 receptor-mediated. In ovalbumin sensitized guinea-pigs, inhaled ovalbumin produced early and late asthmatic responses, inflammatory cell influx and airway hyperreactivity to histamine. These were inhibited by dexamethasone. Bradykinin caused bronchoconstriction without using metabolism inhibitors, indicating airways hyperreactivity to bradykinin. Parainfluenza-3 and influenza caused inflammatory cell influx and airways hyperreactivity to histamine. These were inhibited by FE999024, MEN16132 and dexamethasone. Parainfluenza-3 virus inoculated into sensitized guinea-pigs exacerbated the response to inhaled ovalbumin, with a prolonged bronchconstriction replacing early and late phases. This was resistant to dexamethasone. This study supports a role for bradykinin in virus-induced lung inflammation and the use of inhibitors of bradykinin for potential treatment of airway inflammation.
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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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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 development of Th2 responses and so down-regulate the asthmatic response. The prevalence of asthma is increasing but the reasons for this are not fully understood. In addition, some patients do not respond adequately to treatment with corticosteroids, currently the most effective anti-inflammatory agents used routinely in human asthma. There is therefore continual interest in developing new therapeutic agents for asthma. A greater understanding of the regulation of inflammatory responses in asthma will assist in the identification of potential targets for therapeutic intervention. The aims of this thesis were (i) to assess the role of the cytokine IL-18 in allergic airway inflammation by determining IL-18 levels in induced sputum in asthmatic subjects in comparison to normal subjects, and by studies in a murine model of allergic asthma using IL-18 gene deficient mice and (ii) to assess the potential antiinflammatory actions of simvastatin and thymosin beta 4 sulfoxide in the murine asthma model. IL-18 is a pro-inflammatory cytokine which can promote IFN-y secretion and, in association with IL-12, enhance the development of Thl responses. However, in some circumstances it may also stimulate Th2 responses. IL-18 therefore has the potential to suppress or exacerbate allergic airway inflammation. The role of IL-18 in both clinical and experimental asthma remains unclear. Statins are inhibitors of the rate-limiting enzyme, 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, in cholesterol biosynthesis. As such they have been widely used as cholesterol lowering agents in clinical practice. They have previously been shown to have anti-inflammatory properties independent of their cholesterol-lowering ability in clinical studies of atherosclerotic disease and in animal models of Thlmediated inflammation. Thymosin beta 4 sulfoxide (T~4S0) is a 5 kDa peptide. Intracellularly its principal activity is to regulate actin polymerization. Corticosteroid treatment of monocytes in vitro induces the release of T~4S0 extracellularly, where it can inhibit neutrophil chemotaxis. Exogenous administration of T~4S0 has been shown to reduce neutrophilic inflammation in animal models. In this study it is shown that IL-18 is detectable in induced sputum fluid and IL-18 mRNA is expressed in induced sputum cells from asthmatic and nOlmal subjects. IL- 18 protein levels in induced sputum, and IL-18 mRNA expression in induced sputum cells were not significantly different between these groups. IL-18 production was localised to sputum macrophages. However, cigarette smoking significantly reduced IL-18 levels in induced sputum fluid in both asthmatic and normal subjects. In asthmatics, but not normal subjects, the reduction in IL-18 levels in sputum fluid was associated with reduced IL-18 mRNA expression in induced sputum cells. A murine model of allergic asthma, using BALB/C mice sensitised and challenged with ovalbumin (OVA), was used to examine the role of IL-18 in allergic responses in vivo. IL-18 gene knockout (ko) had significantly reduced bronchoalveolar lavage (BAL) total cell count and eosinophilia compared to wild-type (WT) mice. IL-18 ko mice had reduced IL-4 expression in thoracic lymph nodes, as assessed by quantitative peR, and significantly reduced OVA-specific IL-4 secretion from thoracic lymph node cultures assessed by ELISA. Serum OVA-specific IgG 1, IgG2a and IgE and total IgE levels were not significantly different between IL-18 ko and WT mice. The murine model of allergic asthma was also used to examine the anti-inflammatory activities of simvastatin and T~4S0 in a Th2-mediated, eosinophilic condition. Simvastatin treatment, either orally or intraperitoneally, and T~4S0 intraperitoneally reduced the total inflammatory cell infiltrate and eosinophilia in BAL fluid in response to inhaled OV A challenge. At higher doses of simvastatin intraperitoneally, a histological reduction in inflammatory infiltrates in the lungs was observed. Treatment with simvastatin intraperitoneally, but not orally, and T~4S0 were also associated with a reduction in IL-4 and IL-5 levels in BAL fluid. OVA-induced IL-4 and IL-5 secretion was reduced in thoracic lymph node cultures from both simvastatin-treated and T~4S0-treated mice. Neither simvastatin nor T~4S0 treatment altered serum total IgE or OVA-specific IgG 1 and IgG2a levels. The results described show that IL-18 can be detected in the induced sputum fluid of asthmatic and normal subjects and that cigarette smoking significantly reduces its levels. Studies in a murine model of allergic asthma suggest that IL-18 has a proinflammatory role in allergic airway inflammation, at least in part through its ability to induce IL-4 secretion. Both simvastatin and thymosin beta 4 sulfoxide had convincing anti-inflammatory properties in the murine model of asthma used, and these agents, or related compounds, may have therapeutic potential in human asthma.
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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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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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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 response to viral infection. The viral mimic poly(I:C) increased Pellino-1 protein and gene expression in HBEpCs. In addition, Pellino-1 gene expression was significantly increased by RV-16 and RV-1B infection in primary bronchial epithelial cells from COPD patients. Pellino-1 knockdown in HBEpCs led to a reduction in NF-κB regulated cytokines CXCL8, IL-1α and β gene expression and release of CXCL8 in response to poly(I:C) while having no measurable effect on IFNβ mRNA expression. Furthermore, the transient knockdown of Pellino-1 resulted in the decrease in IKKα/β phosphorylation. The role for Pellino-1 in the non-canonical NF-κB pathway was also investigated and while Pellino-1 knockdown did not alter the expression of the non-canonical NF-κB precursor protein NFKB1 following poly(I:C) stimulation, NFKB2 protein expression was suppressed. In contrast to Pellino-1 knockdown, the transient knockdown of NFKB2 resulted in significant increase in CXCL8 mRNA and protein expression and in turn did not regulate Pellino-1 mRNA expression to poly(I:C). These data suggest that following viral infection in airway epithelial cells, TLR3 activation culminates in the up-regulation of Pellino-1 leading to an increase in NFKB2 expression, resulting in the suppression of NF-κB specific gene transcription. In addition to activating non-canonical NF-κB, NFKB1 regulates the activation of ERK signalling via MEK1. Treatment of HBEpCs with MEK1 inhibitors, PD98059 and U0126, resulted in a significant reduction in Pellino-1 protein and gene expression which led to the suggestion of ERK as a potential Pellino-1 regulator. Proteomics analysis of primary epithelial cells obtained from COPD patient airways further identified a potential novel mechanism of action for Pellino-1 in the NF-κB signalling pathway, wherein it Pellino-1 may inhibit A20’s negative regulatory role or its adaptor proteins TNIP1 or TAX1BP. Taken in combination these data support Pellino-1 as a potential target to down-regulate neutrophilic inflammation whilst retaining antiviral immunity by selectively mediating the TLR3 TRIF-dependent NF-κB/MAPK pathway and not TLR3-mediated IRF3 and IFNβ activation.
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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 of cellular processes; the γ and δ isoforms of the enzyme are of particular importance in leucocyte migration, development and activation. There is increasing evidence for upregulation of this pathway in COPD.Aims: (1) To test the safety of the use of inhaled LPS in patients with COPD for use as a model of exacerbation and to investigate the systemic and airway inflammatory response in vivo. (2) To investigate the action of PI3 kinase enzyme inhibitors and dexamethasone in vitro on neutrophilic inflammation in COPD patients during the stable state and exacerbations. Methods: (1) 12 patients with mild to moderate COPD inhaled 5µg LPS; safety measurements and airway and systemic biomarkers were collected up to 24 hours post inhalation. (2) The effect of PI3 kinase enzyme inhibitors and dexamethasone on MMP-9 and ROS release from peripheral and airway neutrophils from stable COPD and exacerbations was examined in vitro. The effect of PI3 kinase enzyme inhibitors and dexamethasone on cytokine release from peripheral neutrophils from stable COPD patients was also investigated. Results: (1) Inhaled LPS (5µg) caused a significant fall in FEV1 and increase in sputum neutrophil numbers. There was an associated increase in systemic IL-6, CRP and CC-16, all with differing temporal patterns. No patients reported any significant symptoms. (2) PI3 kinase enzyme inhibitors significantly reduced MMP-9 and ROS release from airway and peripheral neutrophils from COPD patients in the stable state and during exacerbations; dexamethasone had minimal effect. Cytokine release from peripheral neutrophils from COPD patients in the stable state was also significantly inhibited by PI3 kinase enzyme inhibitors and dexamethasone. Conclusions: (1) Inhaled LPS in patients with COPD is a safe model to induce acute on chronic neutrophilic inflammation and therefore could be used as a model to study COPD exacerbations. (2) PI3 kinase enzyme inhibitors reduce COPD neutrophil MMP-9, ROS and cytokine release in vitro and are therefore are a promising new anti-inflammatory pharmacotherapy.
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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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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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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 these studies was to investigate the genetic variability of the CC16 and SCGB3A2 genes and their influence on airway inflammatory disease. The main hypothesis was that genetic variability in the genes for CC16 and SCGB3A2 exert an influence on airway inflammatory disease. Three populations were investigated: (1) a paediatric case control population (n=99), (2) an unselected birth cohort followed longitudinally at ages 1 month (n=244), six (n=123) and 11 years (n=195) and (3) an unselected Aboriginal Australian population (n=251). The case-control population was screened for novel DNA sequence variants in the CC16 promoter and the SCGB3A2 5’UTR and exons. No novel sequence variants were identified in the CC16 promoter and two were identified in the SCGB3A2 5’UTR (G- 811A and G-205A). A single nucleotide polymorphism previously identified in the CC16 gene (A38G) and the two polymorphisms identified in the SCGB3A2 gene were genotyped in both unselected populations. Genotype/phenotype associations were identified with adjustment for potential confounders such as age, gender, height and maternal tobacco smoking, where appropriate. This was due to the contribution of these factors to the aetiology of asthma, atopy and related phenotypes. All three polymorphism frequencies were significantly different between these two ethnically diverse populations
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Gajewska, Beata Urszula Jordana Manel. "Generation of immune responses in experimental allergic airway inflammation /." [Hamilton, Ont.] : McMaster University, 2004.
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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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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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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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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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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 ventilate patients. The mechanisms, which mechanical ventilation induces airway inflammation, are complex processes and cover a wide range of spatial scales. The multiscale model of the airway have been developed combining the computational models at organ, tissue, and cellular levels. A model at the organ level was used to study behaviors of the airway during mechanical ventilation. Strain distributions in each layer of the airway were investigated using a model at the tissue level. The cellular inflammatory responses during mechanical ventilation were investigated through the cellular automata (CA) model incorporating all biophysical processes during inflammatory responses. The multiscale modeling framework started by obtaining airway displacements from the organ-level model. They were then transferred to the tissue-level model for determining the strain distributions in each airway layer. The strain levels in each layer were then transferred to the cellular-level model for inflammatory responses due to strain levels. The ratio of the number of damage cells to healthy cells was obtained through the cellular-level model. This ratio, in turn, modulated changes in the Young’s modulus of elasticity at the tissue and organ levels. The simulation results showed that high tidal volume (1400 cc) during mechanical ventilation can cause tissue injury due to high concentration of activated immune cells and low tidal volume during mechanical ventilation (700 cc) can prevent tissue injury during mechanical ventilation and can mitigate tissue injury from the high tidal volume ventilation. The multiscale model developed in this research could provide useful information about how mechanical ventilation contributes to airway inflammation so that a better strategy to ventilate patients can be developed.
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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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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 present a cross-sectional and longitudinal study using dual energy x-ray absorptiometry measurements of body composition and have shown that airway bacterial load and inflammation are independent of body composition changes, and that loss of skeletal muscle is not associated with accelerated airway inflammation or lung function decline. Within a multi-centre exacerbation cohort study I have shown that sputum bacterial load is only weakly associated with quadriceps muscle strength in stable COPD. In addition I have shown only a small, short-lived reduction in quadriceps strength at exacerbation, suggesting that community managed exacerbations may have limited impact on long term decline in muscle and physical function in COPD patients. Finally, I present the results of a single centre study that has shown that air trapping measured using quantitative computed tomography (QCT) makes the strongest unique contribution to airflow obstruction in COPD. Moreover, H. influenzae bacterial load is related to QCT measured small airways disease, and this association is independent of the amount of neutrophilic airways inflammation. In summary, within this thesis I provide data demonstrating significant relationships between H. influenzae, airway inflammation and lung structural changes in COPD. By contrast, my findings suggest that inflammation, and in particular overspill of pulmonary inflammation is not a key pathophysiological mechanism leading to skeletal muscle depletion or dysfunction in COPD.
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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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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 lung mechanics can affect the airway physiology in order to assess the relevance of different animal models of asthma. We have investigated the effects of changing different components of the lung mechanical measurements, such as administering bronchoconstrictive agents via inhalation or intravenously and implementing deep inhalation in animals with airway inflammation. We have also investigated the relation between airway inflammation and oxidative stress. We found that the formation and time-course of F2-isoprostanes, a marker of oxidative stress, and tissue damage were associated with the degree of inflammation and with the degree of heterogeneous airway airflow. Finally we wished to investigate the hypothesis that nitric oxide (NO) may interact with glucocorticoid (GC) treatment because we see a potential for finding new strategies to increase the therapeutic effect in poor responders or patients resistant to GC treatment. NO plays a central role in physiological regulation of the airway function, and is involved in asthma. We found that the concomitant administration of NO and GC attenuated the airway reactivity more than either treatment alone. In conclusion, with the information presented in this thesis, we hope to contribute to the development of better experimental tools and to improved understanding of murine models of asthma for investigating and understanding the underlying pathophysiology of asthma.
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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 study of 32 patients with stable asthma, 25 patients with acute asthma and 25 controls. NO was significantly increased in stable asthma compared with controls (p=<0.01). EBC pH was significantly lower in stable asthma than controls (p=<0.05) and there was a further decrease in acute asthma (p=<0.01). CO and EBC nitrite were not elevated in stable or acute asthma. Induced sputum differential cell counts were investigated in a cross-sectional study of patients with stable asthma (n=42), acute asthma (n=11), chronic obstructive pulmonary disease (n=26), bronchiectasis (n=14) and healthy controls (n=25). The percentage of eosinophils was significantly greater in stable asthma and acute asthma compared with other groups (p=<0.01). There was no difference in the percentage of eosinophils between patients with mild/moderate asthma and severe asthma. However, sputum neutrophil percentage was higher in severe persistent asthma (p=<0.01). To investigate the sensitivity of these markers to short term changes in airway inflammation, serial measurements were made during the resolution of an acute exacerbation of asthma. Exhaled NO decreased and EBC increased by day 7-9 of an exacerbation. The changes in these markers lagged behind changes in FEV1, suggesting that AI persisted beyond the principal period of bronchoconstriction.
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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 of NK cells in the bronchoalveolar lavage (BAL) increased over the time course of HDM challenge and followed a similar trend to eosinophils and Th2 cells. Airway NK cells were activated and expressed NKG2D and granzyme B. In addition, expression of the NKG2D ligand (MULT-1) was upregulated in the lungs of mice treated with HDM. To determine the importance of the NKG2D receptor in allergic inflammation, the HDM model was tested on NKG2D knock out (KO) mice. There was a dramatic reduction in the extent of the inflammatory response in the absence of this receptor, including a reduction in BAL eosinophilia, Th2 responses and serum IgE. Adoptive transfer of wild type (WT) NK cells into NKG2D KO mice restored allergic inflammatory responses to HDM, whereas transfer of granzyme B-/- NK cells did not, demonstrating the requirement for NK cell expression of NKG2D and granzyme B. Detailed phenotypic analysis of NKp46+ cells in the HDM model showed that NKp46+ cells in BAL and lung consisted of RORγt+ and RORγt- subsets. NKp46+RORγt- cells resembled conventional NK cells as they express NKG2D and granzyme B, however NKp46+RORγt+ had similar phenotype to type-3 innate lymphoid cells (ILC3) cells and produced Th2 cytokines upon HDM challenge. We have shown for the first time that NK cells promote allergic lung inflammation via NKG2D and granzyme B production. We have also described for the first time the presence of NKp46+RORγt+ cells in the airways and lung which identifies potential novel therapeutic targets.
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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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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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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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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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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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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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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 contributes to worsening respiratory health, this thesis will consider first immunity of the normal airway and the interactions with vitamin D and then discuss the pathophysiology of CF and the role of vitamin D on the innate immune system within CF. The role of vitamin D on infection and inflammation in the airways of infants with CF is explored and the impact of Vitamin D levels seen immunologically and functionally over the first year of life is described. Finally the role of vitamin D as an immunomodulatory molecule is explored in a greater range of CF disease severity and age. Through the various parameters explored, in different CF patient populations, the conclusion remains the same; vitamin D deficiency is not associated with increased infection, greater inflammation nor a worse clinical outcome. The possible reasons for the lack of any relationship are discussed in the final chapter; either a missed signal because the levels studied were on the low or high flat parts of a 2 sigmoid relationship thus effects seen only in really severe deficiency or because supra-high levels are needed to see any effect, the effect being lost in the inflammation seen within the CF airway or a true lack of relationship.
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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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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 cytokines such as IL-33. Little is known about whether ST2 is expressed on these cells and what function IL-33 responsive ECs may have in Th2 diseases. Soluble ST2 (sST2) has emerged as a biomarker correlating with disease activity in cardiovascular disease. It is not known if there is a clear association between sST2 and asthma, nor whether measurable IL-33 concentrations are present and if so, their association with disease severity. The influence of smoking and corticosteroid treatment on these parameters has also not been determined. Aim: To ascertain the levels of systemic sST2 and IL-33 in asthmatic patients. To determine cytokine, chemokine and airway dynamics of IL-33-driven innate airway inflammation. To determine the role of epithelial cells in IL-33-driven innate airway inflammation. To investigate the function of ST2/IL-33 axis in the innate and adaptive responses in allergic airways inflammation and asthma. Methods and Results: sST2 and IL-33 levels in plasma of never smokers, ex-smokers and smokers were determined by immunoassay before and after a corticosteroid trial. Corticosteroid treatment resulted in increased sST2 levels in all smoking status patient groups; there was no effect attributable to smoking. Time course and dosage interval experiments were performed in mice treated with intranasal IL-33. IL-5, IL-13, eotaxin/CCL11 and eotaxin2/CCL24 mediated eosinophilic airway inflammation (AI). Treatment of mice with both anti- CCL11 and -CCL24 partially ameliorated the AI. IL-4 gene deficient mice were protected from IL-33-induced inflammation. BALB/c mice displayed airways hyperreactivity following IL-33 treatment. Murine, human cell line and primary human ECs were assessed for ST2 expression by immunohistochemistry and fluorescence activated cell sorting (FACS). ST2 expression was clearly demonstrated in the ECs. Subsequently ECs were treated with IL-33 in an in vitro setting including in a pseudostratifed epithelium model. ECs produced a range of inflammatory and angiogenic mediators in response to IL-33. In particular IL-33 driven EC-derived VEGF promoted angiogenesis in vitro. Intranasal IL-33 induced increased endothelial cells and vascular remodelling in vivo. Experimental allergic airways inflammation (AAI) was generated in BALB/c mice which were co-treated with IL-33 or PBS at allergen sensitisation. IL-33 induced the polarisation of IL-5+IL-4- T cells in the draining lymph nodes and these mice developed more severe inflammation. AAI was induced in WT, ST2-deficient, IL-4-deficient and ST2/IL-4 deficient mice. These experiments showed IL-4 was necessary for generation of AAI which could not be overcome by ST2-pathway stimulation in an adjuvant-free model. Conclusions: The data presented further extends the current understanding of the ST2/IL-33 axis in the innate and adaptive aspects of Th2 inflammation in AAI and asthma. In particular the hierarchy of mediators and cells involved in Th2 inflammation, including at the sensitisation phase, have been explored. This identifies ST2/IL-33 as a potential target in the development of biological therapies for asthma.
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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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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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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 severe asthma patients. I have shown that airway structural changes such as bronchiectasis and bronchial wall thickening are common and demonstrate association with disease duration and airflow obstruction. I then present a study describing airway and densitometry phantom models that were developed to study errors associated with quantitative airway morphometry and lung densitometry and device validation and standardisation methods for quantitative CT indices. In the next quantitative cross-sectional study, I report for the first time that right upper lobe apical bronchus (RB1) percent wall area (%WA) was associated with the preceding burden of neutrophilic inflammation over time measured by repeated sputum analysis. RB1 dimensions were not significantly different in four severe asthma phenotypes determined based on clinical and physiological indices. I also present a study demonstrating a decrease in RB1 wall dimensions after 1 year of treatment with mepolizumab (anti-IL-5) compared to placebo providing strong evidence in favour of the eosinophils playing a key role in airway remodelling determined by CT. Finally, I report for the first time three distinct asthma phenotypes identified based on CT assessed proximal and distal airway remodelling. Temporal assessment in severe asthma subjects demonstrates increase in RB1 wall dimensions over time but no change in RB1 lumen dimensions. These findings underpin the role of CT in multi-dimensional phenotyping of severe asthma.
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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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