Dissertations / Theses on the topic 'Airway eosinophilia'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 28 dissertations / theses for your research on the topic 'Airway eosinophilia.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse dissertations / theses on a wide variety of disciplines and organise your bibliography correctly.
Birrell, Mark Andrew. "Characterisation of animal models of airway eosinophilia." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408172.
Full textDe, Campo Benjamin. "The influence of PAR activators on allergen-induced pulmonary eosinophilia and hyperresponsiveness in mice /." Connect to this title, 2007. http://theses.library.uwa.edu.au/adt-WU2008.0060.
Full textBrightling, Christopher. "Airway eosinophilia in chronic cough, asthma and chronic obstructive pulmonary disease : an immunopathological feature of disease and a marker of response to corticosteriods." Thesis, University of Leicester, 2002. http://hdl.handle.net/2381/29409.
Full textKottyan, Leah Claire. "Airway Acidification in Asthma." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1280778640.
Full textHumbles, Alison Anita. "The relationship between the generation of an eosinophil-selective chemoattractant, ecotoxin and eosinophil accumulation in vivo." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267879.
Full textEltboli, Osama M. I. "Eosinophilic airways inflammation in Chronic Obstructive Pulmonary Disease." Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/32546.
Full textHallsworth, Matthew Pearce. "GM-CSF and eosinophil survival in asthma." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341883.
Full textFulkerson, Patricia C. "A Critical Role for Eosinophils and CCR3 Signal Transduction in Allergic Airway Disease." University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1120337075.
Full textLavinskienė, Simona. "Peripheral blood neutrophil and eosinophil activity during allergen-induced late-phase airway inflammation in asthma." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2015. http://vddb.library.lt/obj/LT-eLABa-0001:E.02~2014~D_20150106_083713-90371.
Full textMokslininkai neabejoja, jog eozinofilai ir neutrofilai yra vienos svarbiausių ląstelių, dalyvaujančių astmos patogenezėje, kurią labiausiai atspindi vėlyva kvėpavimo takų uždegimo fazė, išsivystanti praėjus kelioms valandoms po alergeno įkvėpimo. Pasaulinėje literatūroje publikuojami darbai, nagrinėja atskirus kvė¬pavimo takų neutrofilų ir eozinofilų aktyvumo pokyčius. Ypač mažai darbų apie periferinio kraujo neutrofilų ir eozinofilų funkcijas bei jų ryšį su šių ląstelių pagausėjimu kvėpavimo takuose, sergant astma. Taip pat nėra tyrimų, vertinančių periferinio kraujo uždegimo ląstelių (neutrofilų ir eozi¬nofilų) funkcijų alergeno sukeltos vėlyvos fazės kvėpavimo takų uždegimo metu. Todėl šio tyrimo tikslas buvo įvertinti periferinio kraujo neutrofilų ir eozinofilų funkcinį aktyvumą alergeno sukeltos vėlyvos fazės kvėpavimo takų uždegimo metu sergant astma. Tyrimo metu nustatėme, kad įkvėptas alergenas aktyvina periferinio kraujo neutrofilų ir eozinofilų funkcijas - chemotaksį, fagocitozę, reaktyvių deguonies formų susidarymą, degranuliaciją bei silpnina apoptozę vėlyvos fazės kvėpavimo takų uždegimo metu. O šių ląstelių aktyvumo pokyčiai yra susiję su kvėpavimo takų neutrofilija ir eozinofilija. Moksliniame darbe pateikiami rezultatai suteikia naujų duomenų apie sergančiųjų alergine astma periferinio kraujo neutrofilų ir eozinofilų funkcinių savybių ypatumus ir parodo jų pokyčius alergeno sukeltos vėlyvos fazes kvėpavimo takų uždegimo metu.
Shahana, Shahida. "Cell Contacts and Airway Epithelial Damage in Asthma." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4775.
Full textNutku, Turkan Esra. "Role of IL-12 and IL-18 in regulation of eosinophil function in allergic airway inflammation." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85633.
Full textThe general aim of this study was to determine the effect of IL-12 and IL-18 on eosinophil functions. Results from this thesis demonstrate that eosinophils express functional receptors for IL-12 and IL-18. Acting alone or in synergy, IL-12 and IL-18 induced eosinophil apoptosis, in vitro. The apoptotic effect of IL-12 was reversed by IL-5, suggesting that IL-5 and IL-12 have counter-regulatory effects on eosinophil survival. Our regulation studies demonstrated that Phorbol-Myristate-Acetate (PMA) induced optimal expression of IL-18 and IL-12 receptors by eosinophils. IL-18 receptor expression by eosinophils was markedly increased following stimulation with interferon (IFN)-gamma, Tumor Necrosis Factor (TNF), or IL-12. Up-regulation of IL-18 receptor upon IL-12 stimulation was particularly important, which may explain IL-12 and IL-18 synergy on eosinophil apoptosis. We also investigated IL-12 and IL-18 expression by eosinophils. Eosinophils did not express IL-18. However, there was constitutive IL-12 expression by eosinophils. Release of IL-12 was also confirmed in eosinophil supernatants, which suggested an autocrine mechanism of IL-12 action on eosinophils.
Extending our understanding of the role of IL-12 and IL-18 in allergic inflammation, we have defined a novel pathway by which IL-12 and/or IL-18 may actually regulate eosinophils functions, and exert an inhibitory effect on eosinophil survival. Our findings provide critical new insights into mechanisms regulating eosinophil survival. To gain an even more detailed understanding of regulatory signals mediating eosinophil survival, we need to define the mechanisms involved in IL-12 and IL-18 signalling. We have just begun to identify the molecules involved, and these include IL-12 and IL-18 receptors. Activation via IL-12 and/or IL-18 receptor-mediated mechanisms may provide a novel strategy for reducing the numbers or inhibiting the function of these cells in allergic diseases or other diseases characterized by increased numbers of, or mediators from, eosinophils.
Безруков, Л. О., and Є. П. Ортеменка. "The role of airway hyperreactivity and type of acetylation as a predioctor of eosinophilic asthma in school-age children." Thesis, Матеріали НПК [«Актуальні питання діагностики та лікування алергічних і неалергічних захворювань респіраторної системи у дітей» із сателітним симпозіумом «Сучасні технології та інновації викладання педіатрії та пульмонології»], 2016. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/13139.
Full textHaji, Sadeghi Mahboobeh. "The emerging role of the eosinophil and its measurement in chronic cough : airway inflammation in chronic cough." Thesis, University of Hull, 2017. http://hydra.hull.ac.uk/resources/hull:16543.
Full textSexton, Darren W. "Elucidation of the mechanisms involved in the recognition and engulfment of apoptotic human eosinophils by airway epithelial cells." Thesis, University of Aberdeen, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252134.
Full textIio, Jun. "Lipid A analogue, ONO-4007, inhibits IgE response and antigen-induced eosinophilic recruitment into airways in BALB/c mice." Kyoto University, 2002. http://hdl.handle.net/2433/149702.
Full textAbdelaziz, Muntasir Mustafa. "Role of airway epithelial cells in eosinophil activation and recruitment and the influence of non-steroid anti-inflammatory therapeutic agents." Thesis, Queen Mary, University of London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313838.
Full textMacKenzie, Jason Roderick, and Jason Mackenzie@ipaustralia gov au. "The Role of Eosinophils in the Regulation of CD4+ T helper 2 Regulated Inflammation." The Australian National University. The John Curtin School of Medical Research, 2004. http://thesis.anu.edu.au./public/adt-ANU20051007.121844.
Full textPatelis, Antonios. "IgE sensitization against food allergens : Natural history, relation to airway inflammation and asthma." Doctoral thesis, Uppsala universitet, Institutionen för medicinska vetenskaper, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-251396.
Full textMwanthi, Muithi. "PAK1's regulation of eosinophil migration and implications for asthmatic inflammation." Thesis, 2013. http://hdl.handle.net/1805/3786.
Full textMore than 300 million people world-wide suffer from breathlessness, wheezing, chest tightness, and coughing characteristic of chronic bronchial asthma, the global incidence of which is on the rise. Allergen-sensitization and challenge elicits pulmonary expression of chemoattractants that promote a chronic eosinophil-rich infiltrate. Eosinophils are increasingly recognized as important myeloid effectors in chronic inflammation characteristic of asthma, although few eosinophil molecular signaling pathways have successfully been targeted in asthma therapy. p21 activated kinases (PAKs), members of the Ste-20 family of serine/threonine kinases, act as molecular switches in cytoskeletal-dependent processes involved in cellular motility. We hypothesized that PAK1 modulated eosinophil infiltration in an allergic airway disease (AAD) murine model. In this model, Pak1 deficient mice developed reduced inflammatory AAD responses in vivo with notable decreases in eosinophil infiltration in the lungs and broncho-alveolar lavage fluids (BALF). To test the importance of PAK1 in hematopoietic cells in AAD we used complementary bone marrow transplant experiments that demonstrated decreased eosinophil inflammation in hosts transplanted with Pak1 deficient bone marrow. In in vitro studies, we show that eotaxin-signaling through PAK1 facilitated eotaxin-mediated eosinophil migration. Ablating PAK1 expression by genetic deletion in hematopoietic progenitors or siRNA treatment in derived human eosinophils impaired eotaxin-mediated eosinophil migration, while ectopic PAK1 expression promoted this migration. Together these data suggest a key role for PAK1 in the development of atopic eosinophil inflammation and eotaxin-mediated eosinophil migration.
Simpson, Jodie Louise. "Inflammatory mechanisms in non-eosinophilic asthma." Thesis, 2005. http://hdl.handle.net/1959.13/1418343.
Full textAsthma is defined as a 'chronic inflammatory disorder of the airways, which involves many cells and cellular elements". Eosinophilic airway responses have been well characterised in asthma, and recently non-eosinophilic forms of asthma have been identified. The non-eosinophilic asthma phenotype is characterised by clinical symptoms of asthma and airway hyperresponsiveness occurring in the absence of raised sputum eosinophils. The non-eosinophilic pattern of inflammation has been reported across whole spectrum of asthma severity including mild asthma, persistent asthma and severe refractory asthma. The aim of this thesis was to investigate the characteristics and inflammatory mechanisms of non-eosinophilic asthma. The recognition of non-eosinophilic asthma using induced sputum eosinophil counts was examined. The role of proteolytic enzymes and innate immune activation as potential mechanisms of non-eosinophilic asthma were also examined in subjects with stable persistent symptomatic asthma treated with inhaled corticosteroids and healthy controls. A definition of non-eosinophilic asthma based upon a normal sputum eosinophil proportion was found to be reproducible. This was a heterogeneous inflammatory phenotype containing a group with increased neutrophils (neutrophilic asthma) and a group with normal levels of neutrophils and eosinophils termed paucigranulocytic asthma. Eosinophilic asthma was characterised by the presence of high levels of active matrix metalloproteinase-9 and low levels of neutrophil elastase. Neutrophilic asthma was characterised by high levels of neutrophil elastase and almost no active matrix metalloproteinase-9. Subjects with neutrophilic asthma also had evidence of chronic bacterial colonisation of the airways, high levels of airway endotoxin and innate immune activation with increased expression of the toll-like receptors 2 and 4 and increased surfactant protein A in sputum. Airway inflammation is heterogenous and can be classified into phenotypes based upon abnormal levels of sputum neutrophils and eosinophils. More than 50% of symptomatic persistent asthma is non-eosinophilic in nature, with more than 20% of these subjects having a neutrophilic airway inflammation and the remainder exhibiting a paucigranulocytic asthma. Innate immune activation is an important inflammatory mechanism in neutrophilic asthma, which may explain the increased expression of pro-inflammatory cytokines and proteolytic enzymes in neutrophilic asthma. Over 30% of subjects with persistent asthma have a persistent eosinophilia despite receiving high doses of inhaled corticosteroids. The findings of this thesis have important implications for the management, treatment and monitoring of asthma and support the inclusion of a measure of airway inflammation in the clinical assessment of asthma to guide therapy and further investigation into airway disease.
Chou, Kun-Ta, and 周昆達. "Detection of Eosinophilic Airway Inflammation in Chronic Obstructive Pulmonary Disease." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/asr7ka.
Full text國立陽明大學
臨床醫學研究所
107
Despite COPD (chronic obstructive pulmonary disease) and asthma are usually considered two distinct diseases, a substantial portion of patients present with features of both diseases. COPD with eosinophilic airway inflammation may represent a unique phenotype of asthma-COPD overlap, with shared features of COPD and asthma. A convenient test or tool is urgently needed to detect such population. Hence, we examined the role of exhaled nitric oxide (eNO) and an enhanced bronchodilator response in identifying COPD patients with sputum eosinophilia. The first part of the thesis, we prospectively enrolled 90 COPD patients without past medical history of asthma or allergic diseases, whose eNO, lung function and cellular profile/Eosinophil cationic protein/Immunoglobulin E (IgE) of induced sputum were measured. Eosinophil cationic protein and IgE in venous blood were also determined. Comparison between subjects with and without sputum eosinophilia (>3%) was made. Patients with sputum eosinophilia (29/90=32%) had significant higher levels of eNO (29 vs. 18 ppb, p=0.01) compared to those without it. The sputum eosinophil level was significantly correlated to the eNO level (r=0.485, p<0.001). The eNO level at the cut-off of 23.5 ppb had the maximum sum of a sensitivity (62.1%) and a specificity (70.5%). The unadjusted and adjusted odds ratio (OR) of a higher eNO level (>23.5 ppb) in prediction of sputum eosinophilia is 3.909 (CI=1.542-9.910, p =0.004) and 4.329 (CI=1.306-14.356, p=0.017), respectively. The last part of the thesis looked into the relationship of bronchodilator reversibility and eosinophilic airway inflammation in COPD. We retrospectively analyzed 264 stable COPD patients without a past history of asthma, showing 82 (31.1%) patients had sputum eosinophilia and FEV1 reversibility was weakly correlated to the sputum eosinophil level (r=0.162, p=0.008). Patients with FEV1 increment > 0.4L & >15% had a higher sputum eosinophil level (6.11 vs 1.02%, p=0.049) whereas the level did not differ if stratified by FEV1 increment >0.2L & >12%. Very positive FEV1 reversibility (>0.4L & >15%) in prediction of sputum eosinophilia remained significant after adjustment of age, baseline FEV1 and FVC (OR: 4.262, p=0.029). The ROC analysis showed AUC was 0.58 (p=0.034) and FEV1 increment > 0.4L & >15% had a positive predictive value of 63.6% and an overall accuracy of 70.1%. In conclusion, eNO can predict presence of eosinophilic airway inflammation in COPD patients whereas an enhanced bronchodilator response can barely meet the need.
LIU, CHIEN-YU, and 劉千玉. "Licochalcone A Attenuated Airway Hyperresponsiveness And Eosinophilic Infiltration In OVA-inducedAsthmatic Mice." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/458hbg.
Full text長庚科技大學
健康產業科技研究所
106
Licochalcone A, a flavonoid, was isolated from the root of Glycyrrhiza glabra. Licochalcone A was reported to have anti-malarial, anti-tumor, anti-bacterial, antiviral and anti-inflammatory effect. The aim of this study was to investigate whether licochalcone A suppressed eosinophil infiltration and airway hyperresponsiveness (AHR) in asthmatic mice, and decreased the inflammatory response and oxidative stress in tracheal epithelial cells. BALB/c mice were sensitized and challenged with ovalbumin to induce allergic asthma in mice. These asthmatic mice were given various doses of licochalcone A by intraperitoneal injection. Additionally, activated human tracheal epithelial cells (BEAS-2B cells) and adenocarcinomic human alveolar basal epithelial cells (A549 cells) were treated with licochalcone A, and evaluated for levels of proinflammatory cytokines and chemokines. We found that licochalcone A significantly decreased AHR, and T-helper type 2 (Th2) cell over expression, and suppressed goblet cell hyperplasia, eosinophil infiltration, and inflammatory response in the lung tissue of asthmatic mice. Licochalcone A also reduced the levels of Th2 cytokines and chemokines in bronchoalveolar lavage fluid, and suppressed OVA-IgE production in serum. Furthermore, licochalcone A treatment of activated BEAS-2B cells and A549 cells decreased production of proinflammatory cytokines and eotaxins, as well as suppressed ICAM-1 expression and thus adhesion of eosinophils to inflammatory BEAS-2B cells and A549 cells in vitro. Our findings suggest that licochalcone A can improve allergic asthma in mice, and therefore has therapeutic potential in humans.
Lien, Pei-Chun, and 連培均. "Regulatory effects of human eosinophil cationic protein in airway inflammation." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/17791128857956557295.
Full textClark, Kristopher. "Eosinophil activation in a mouse model of allergic airways disease." Thesis, 2003. http://hdl.handle.net/1885/148528.
Full textYang, Ming. "Molecular mechanisms regulating eosinophil migration and airways hyperreactivity in mice." Phd thesis, 2003. http://hdl.handle.net/1885/148761.
Full textEssilfie, Ama-Tawiah. "Modulation of responses in allergic airways disease by Haemophilus influenzae infection." Thesis, 2012. http://hdl.handle.net/1959.13/927983.
Full textAsthma is a common chronic inflammatory disease of the airways that affects over 2.2 million people in Australia. Asthma is a heterogeneous inflammatory disease typically characterised by T helper lymphocyte type 2 (Th2)-mediated eosinophilic inflammation, exaggerated responses to innocuous stimuli, mucus hypersecretion leading to airways obstruction and airway remodelling. These physiological changes result in wheezing, chest tightness, and breathing difficulties. However, it has been established that eosinophilic inflammation is only present in 50% of asthmatic patients. Around 30% of non-eosinophilic asthmatics have neutrophilic rather than eosinophilic inflammation, which is a key feature of neutrophilic asthma. Non-typeable Haemophilus influenzae (NTHi) is a Gram-negative bacterium that is commonly found in the upper respiratory tract of about 75% of healthy individuals. It is normally asymptomatically carried in people, however it may cause otitis media and is a common cause of community-acquired pneumonia. NTHi has also been linked to a number of chronic airway diseases. It has been detected in patients with bronchiectasis, chronic bronchitis and is commonly associated with chronic obstructive pulmonary disease (COPD) exacerbations. It has also recently been associated with neutrophilic asthma, however, the role of NTHi in neutrophilic asthma has not been investigated. Using murine models of NTHi infection and allergic airways disease (AAD), we investigated the relationship between infection and AAD. We showed that NTHi infection induced features of neutrophilic asthma; reduced Th2-mediated eosinophilic inflammation, reduced airways hyper-responsiveness (AHR) compared to eosinophilic AAD, and importantly, significantly increased Th17 responses and neutrophilic inflammation. In the first study it was demonstrated that the combination of infection and AAD reduced the expression of MHC II and CD86 on dendritic cells (DCs), suggesting that infection induced changes in presentation of antigen to naïve T-cells and subsequent adaptive responses. Infection also induced Interleukin (IL)-17 production from innate cells and Th17 cells. Critically, we show that inhibiting IL-17 significantly reduced neutrophilic inflammation in the airways. This highlights the crucial role of IL-17 in infection-induced neutrophilic AAD. The second study showed that the induction of AAD during infection delayed bacterial clearance from the lungs compared to infection alone controls. In contrast to Th2-mediated eosinophilic inflammation, this model of infection-induced neutrophilic AAD was resistant to dexamethasone treatment. All features of infection-induced neutrophilic AAD, including eosinophil and neutrophil influx, antigen-specific IL-5, IL-13 and Interferon (IFN)-γ, NTHi-specific IL-17, and AHR were unchanged with steroid treatment. This study also demonstrated that neutrophil and macrophage activation and function was inhibited in neutrophilic AAD. This lack of innate immune response may enable chronic bacterial infection. The final study investigated clarithromycin, a macrolide, and combination therapy with dexamethasone, as possible treatment strategies for neutrophilic asthmatics. This study demonstrated that clarithromycin alone significantly reduced neutrophil influx and IL-17 responses, but increased Th2-mediated eosinophilic inflammation. However, the combination of clarithromycin and dexamethasone suppressed all key features of AAD, including eosinophilic and neutrophilic inflammation, ovalbumin (OVA)-specific IL-5, IL-13, and IFN-γ, NTHi-induced IL-17, and AHR. These novel findings further the understanding of the potential role of NTHi in the development of neutrophilic asthma. We have identified some mechanisms of how infection may lead to features observed in neutrophilic asthma, and importantly, possible treatment strategies for neutrophilic asthmatics, and perhaps, other neutrophilic airway diseases with evidence of infection.
Gunawardhana, Lakshitha. "Epigenetic regulation of airway inflammation in asthma." Thesis, 2014. http://hdl.handle.net/1959.13/1058797.
Full textAsthma is an inflammatory disease that manifests in the airways. There are an estimated 300 million people worldwide currently suffer from asthma. Common asthma symptoms include dyspnea and wheezing. These are consequences of the reversible airflow obstruction associated with airway inflammation. The symptoms can be mild or can be as severe as life threatening depending on nature of underlying inflammation. Although heredity plays a role in the disease pathogenesis, the high and rising prevalence of asthma, particularly in recent decades highlights a strong influence of the environment. To this end, epigenetic phenomena including alteration of DNA methylation and chromatin structure are likely contributors to the pathogenesis of asthma as well as a plausible source of phenotype heterogeneity. Especially subtle alteration of DNA methylation patterns which occur early in life may impact on disease development. However, the exact role of epigenetic mechanisms in the pathogenesis of asthma and inflammatory phenotypes of asthma are not well understood. This thesis investigates; 1) Alterations in infant peripheral blood DNA methylation profiles associated with pre-natal exposure to maternal asthma, 2) The role of chromatin structure by analysing histone acetyl-transferases (HAT) and histone de-acetylases (HDAC) activity of peripheral blood monocytes in inflammatory phenotypes of adult asthma, 3) Alterations in the DNA methylation profile of peripheral blood monocytes associated with inflammatory phenotype of adult asthma. The primary findings of this thesis are: 1) Maternal asthma during pregnancy is associated with alterations in peripheral blood DNA methylation in infants’. 2) Inflammatory phenotypes of asthma are associated with differential DNA methylation in peripheral blood monocytes. Gene network analyses of these differentially methylated genes revealed distinct molecular pathways, suggesting possible implications in the disease pathogenesis. 3) Neutrophilic asthma is associated with lower HDAC activity and higher HAT activity of peripheral blood monocytes compared to both eosinophilic and paucigranulocytic asthma. Collectively, the findings of this thesis emphasised the significance of epigenetic factors playing a role in the development of asthma and inflammatory phenotypes of asthma. An association of peripheral blood methylation profiles of infants with maternal asthma suggests a potential inheritance of the disease susceptibility. The characteristic alterations of DNA methylation in blood monocytes suggest an underlying epigenetic basis for the inflammatory phenotypes while the differences in HAT/HDAC activity in monocytes further emphasise a role for the epigenome in the development of inflammatory phenotypes. The findings of this thesis warrant further investigation and may help us get one step closer to understanding the role of epigenetics in airway inflammation in asthma.
MacKenzie, Jason Roderick. "The Role of Eosinophils in the Regulation of CD4+ T helper 2 Regulated Inflammation." Phd thesis, 2003. http://hdl.handle.net/1885/47792.
Full text