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Dissertations / Theses on the topic 'Pulmonary infection'
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Moriarty, T. F. M. "Pulmonary infection in cystic fibrosis : microbiology and antibiotic treatment at the site of infection." Thesis, Queen's University Belfast, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432522.
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Field, Tyler Robert. "Anaerobic pulmonary infection in cystic fibrosis : detection, characterisation and treatment." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.479420.
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McManus, T. E. "Viral infection and associated inflammation in chronic obstructive pulmonary disease." Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426766.
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Keir, Pamela Alexandra. "Early responses in the pulmonary phase of Nippostrongylus brasiliensis infection." Thesis, Edinburgh Napier University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270301.
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Wilkinson, Thomas Michael Alan. "The role of airway infection in chronic obstructive pulmonary disease." Thesis, Queen Mary, University of London, 2006. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1897.
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This. thesis examines the role of respiratory bacterial and viral infection in the natural history of Chronic Obstructive Pulmonary Disease. The rationale for this study is basedu pon previous data demonstratingt hat airway bacterial colonisationi s common in stable COPD and that bacterial and viral pathogens are commonly detected at exacerbations. The methodsu sed have involved the careful characterisationa nd clinical follow up of a cohort of patients with moderate to severe COPD in the stable state and at exacerbation. Sampling of airway and systemic compartments enabled the detection of respiratory pathogens and quantification of inflammation. Comparisons between clinical indices and evidence of infection were performed to determine the relationships between bacterial and viral infections and disease outcomes including lung function decline and exacerbation severity. The findings confirmed that lower airway bacterial colonisation is common in stable COPD and is associated with airway inflammation. They demonstrated for the first time a relationship between the degree of bacterial carriage and the rate of disease progression. This study has also described novel evidence for persistence of respiratorys yncytial virus in the lower airway and associationsw ith inflammation and lung function decline and impaired anti-viral immune responsesT. he combined role of human rhinoviral and bacterial infection at exacerbation has been studied and factors influencing responsesto exacerbationt herapy determinedw ith the importance of early initiation of treatment identified. The findings in this thesis indicate that both viral and bacterial pathogens may play an important role in the natural history of COPD and are therefore targets for potentially novel interventions. This work suggests that viral and bacterial infections and their interactions play an important role in modulating airway inflammation in stable disease and at exacerbation thus impacting on both disease progression and exacerbation severity. This work has provided a rationale for future investigation into the mechanisms underlying susceptibility to infection in this important disease.
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Robert, Camille. "Evaluation du potentiel thérapeutique d'un mannodendrimère anti-inflammatoire dans un modèle murin d'infection par Francisella tularensis." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30299/document.
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Francisella tularensis est une bactérie intracellulaire à Gram négatif et l'un des agents les plus infectieux connu à l'heure actuelle, en particulier par voie respiratoire. L'inhalation d'une dizaine de bactéries suffit à provoquer une maladie mortelle : la tularémie pulmonaire. Sa facilité de dissémination par aérosols, ainsi que le caractère létal de cette pathologie, ont contribué à considérer F. tularensis comme une arme biologique potentielle. La tularémie pulmonaire est une infection aigue qui s'accompagne d'une réponse immunitaire inadaptée. F. tularensis infecte en premier lieu les cellules phagocytaires, notamment les macrophages. Alors que ces derniers sont des acteurs majeurs de la défense contre les agents infectieux, de nombreux mécanismes d'échappement permettent à F. tularensis d'éviter ou de résister aux réponses de l'hôte et ainsi de se multiplier et de disséminer dans l'organisme. Ainsi, après un retard initial dans la mise en place de la réponse immunitaire, la présence d'un grand nombre de bactéries et de signaux de danger libérés par les cellules infectées, conduisent au déclenchement d'une réponse inflammatoire excessive. Celle-ci se caractérise par une tempête cytokinique provoquant un recrutement massif de cellules immunitaires, en particulier de neutrophiles, dans les tissus infectés. Les dommages tissulaires associés à cette réponse inflammatoire sont en grande partie responsable de la mortalité associée aux infections pulmonaires par F. tularensis. La tularémie est actuellement traitée par antibiothérapie. Malheureusement, l'absence de symptômes spécifiques de cette maladie rend le diagnostic difficile et, par conséquent, retarde la prescription du traitement adapté. Or, l'efficacité des antibiotiques est considérablement réduite par cette administration tardive. De nouvelles stratégies thérapeutiques sont donc nécessaires pour remplacer ou compléter l'antibiothérapie. Dans ce contexte, nous avons cherché à déterminer si la modulation de la réponse inflammatoire excessive induite par F. tularensis pouvait être bénéfique pour l'hôte infecté et ainsi être utilisée comme thérapie accessoire. L'objectif de mon travail de thèse était d'évaluer les propriétés anti-inflammatoires et le potentiel bénéfice thérapeutique du mannodendrimère 3T (M3T), un composé synthétisé par l'équipe de J. Nigou, dans un modèle murin d'infection pulmonaire par F. tularensis. Le M3T, conçu pour mimer les propriétés anti-inflammatoires d'un glycolipide de la paroi de Mycobacterium tuberculosis, a précédemment montré un effet inhibiteur sur la production de cytokines pro-inflammatoires et le recrutement de neutrophiles dans un modèle murin d'inflammation pulmonaire aigue induite par le LPS. La souche F. novicida, provoquant chez la souris une pathologie similaire à une infection pulmonaire par F. tularensis, a été utilisée comme souche de substitution dans ces travaux. In vitro, nous avons montré que le M3T inhibe la production de cytokines pro-inflammatoires induite par F. novicida dans des macrophages et cellules dendritiques humaines. D'un point de vue mécanistique, l'ensemble des données suggère que le M3T inhibe la réponse inflammatoire induite par F. novicida via le récepteur TLR2, en activant une voie de signalisation dépendante du récepteur DC-SIGN. In vivo, le M3T a été administré par injection intraveineuse 6 h post-infection, puis quotidiennement pendant 3 jours, en combinaison avec un traitement antibiotique sous-optimalFrancisella tularensis is an intracellular Gram negative bacterium and the causative agent of tularemia. It is one of the most infectious agents known to date. Infection by the respiratory route leads to the deadly pulmonary form of tularemia. For these reasons, F. tularensis has been considered for years as a potential biological weapon. Pulmonary tularemia is characterized by an acute infection and a defect in immune responses. Particularly, the innate immune system plays a central role in F. tularensis infection and pathology. Macrophages, key cells of the innate immune system, are the main target for F. tularensis. This bacterium has evolved many strategies to escape host defenses that allow it to replicate within the cells and then disseminate into the whole organism. At this systemic stage, bacteria, along with alarm signals from infected cells, are recognized by innate immune receptors, triggering an inappropriate inflammatory response. The latter is characterized by a cytokine storm leading to a massive recruitment of immune cells, particularly neutrophils, in infected tissue. Tissue damages caused by this inflammation are a major cause of mortality associated with F. tularensis infections. Today, the treatment of tularemia is based on antibiotherapy. However, no specific symptoms can be assigned to pulmonary tularemia making its diagnosis difficult. This delays the administration of an appropriate antibiotiotherapy whose efficacy is therefore decreased. Thus, new therapeutic strategies are needed to replace or complement antibiotics. In this context, we investigated whether reducing the excessive inflammation induced by F. tularensis could be beneficial for the host and be considered as an adjunctive host- directed therapy. The aim of my work was to evaluate the anti-inflammatory properties and the therapeutic potential of mannodendrimer 3T (M3T), a synthetic coumpond designed in the team, in a mouse model of pulmonary infection by F. tularensis. M3T was previously designed to mimic the anti-inflammatory traits of a specific glycolipid from Mycobacterium tuberculosis. It was previously shown to inhibit the production of pro-inflammatory cytokines and neutrophils recruitment in a mouse model of LPS-induced pulmonary inflammation. Here, we used F. novicida as a surrogate for F. tularensis since it induces an identical inflammatory pathology. In vitro, M3T was found to inhibit the production of pro-inflammatory cytokines in human macrophages and dendritic cells infected by F. novicida. M3T modulates inflammatory response triggered by F. novicida via TLR2 most likely by the activation of a DC-SIGN-dependant pathway. In vivo, M3T was administered 6 h post-infection and then, daily for 3 days, by intraveinous injection and combined with a suboptimal antibiotic. This combination increases the survival rate of mice infected with F. novicida as compared to mice treated with antibiotic alone. M3T treatment has no impact on bacterial burden but seems to reduce tissue damages as observed by histological analyses of lungs, liver and spleen of infected mice. Altogether, our data demonstrate that M3T administration provides a therapeutic benefit in a mouse model of pulmonary infection by F. novicida. On a more general perspective our results suggest that targeting inflammation can be considered as an adjunctive treatment in acute pulmonary infections
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Nixon, Lisette Sheena. "Neutrophil function in patients with cystic fibrosis and chronic pulmonary infection." Thesis, Cardiff University, 2003. http://orca.cf.ac.uk/54082/.
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The thesis investigates reasons for a failure of neutrophils to clear pulmonary bacterial infection in cystic fibrosis (CF). Patients with CF experience bacterial colonization of the lungs associated with progressive lung injury and poor prognosis. Neutrophil responsiveness in vitro was determined in patients with CF at different clinical states, and compared to healthy subjects. Neutrophils from the patients were able to phagocytose and kill Pseudomonas aeruginosa effectively, but the presence of sputum sol reduced intracellular killing. Superoxide generation and elastase release in response to fMLP were shown to be reduced in neutrophils from patients with an exacerbation of respiratory symptoms. This was not observed when the cells were stimulated with PMA, which acts intracellularly, rather than through cell surface receptors. There was no difference in the down-regulation of cell surface L-selectin and up-regulation of CD11b in response to fMLP suggesting no alteration in number or function of the fMLP receptors. There was increased adherence to nylon columns by neutrophils from patients with CF. Infection resulted in a greater proportion of band neutrophils, and this correlated with the reduced superoxide generation and elastase release, although it was not possible to separate the band forms to prove this conclusively. Alterations in circulating lipid and fatty acid composition inpatients could potentially affect neutrophil membrane composition and fluidity and therefore signal processing or release of products. The reason for the observed reduced responsiveness appears to be multifactorial. Band cell number post receptor signalling and/or receptor desensitization may result in the observed reduced responsiveness, which returns towards healthy subject levels after treatment of an exacerbation, is likely to be the result of chronic infection.
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Tomlinson, G. S. "Inflammatory responses by monocytes and macrophages in pulmonary sarcoidosis and infection." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1344095/.
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Inflammatory responses by macrophages are essential for host defense, but also underpin the pathogenesis of numerous diseases. I adopted a systems biology approach using transcriptional profiling to investigate monocyte and macrophage inflammatory responses in relation to pulmonary sarcoidosis and infection, to compare alveolar macrophages (AM) and monocyte derived macrophages (MDM), and to probe integrated innate and adaptive immunological responses within the tuberculin skin test (TST). In sarcoidosis I established the importance of prostaglandin endoperoxide synthase (PTGS)2 promoter haplotypes in determining susceptibility to disease across two genetically dissimilar ethnic groups, UK Whites and Afro-Caribbeans, but found no functional effect of promoter haplotype on PTGS2 gene expression, in mononuclear phagocytic cells. In contrast to the widely held view that AM have an anti-inflammatory bias, I show that freshly isolated AM have a striking pro-inflammatory profile that may confound the study of their responses to innate immune stimulation. In human immunodeficiency virus (HIV)/Mycobacterium tuberculosis (Mtb) co-infection I show that HIV-1 infection of macrophages leads to augmented inflammatory responses to Mtb, accompanied by enhanced viral replication, due to deficient induction of anti-inflammatory IL10, via attenuation in mitogen activated protein kinase (MAPK) signalling pathways downstream of TLR2 and dectin-1. These changes were not evident in HIV-1/Streptococcus pneumoniae co-infected macrophages, and the specificity of the effect in Mtb co-infection was mirrored by lower IL10 and higher pro-inflammatory IL1β in HIV-infected patients with pulmonary tuberculosis compared with non-tuberculous infection. Finally, I show that the TST is characterised by Th1 polarised and cytotoxic T cell responses. Distinct innate immune and IFNγ-stimulated gene expression signatures under NFκB and STAT1 transcriptional control and highly enriched for chemokines and MHC class II molecules, provide a mechanism for paracrine amplification of inflammatory responses in the TST. Strikingly, identical responses of lower magnitude were also detectable in clinically negative TST subjects.
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Chidgey, Sharon Michelle. "Airway function, inflammation and pulmonary histopathology following parainfluenza-3 virus infection." Thesis, Cardiff University, 2007. http://orca.cf.ac.uk/55663/.
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Human parainfluenza viruses (PIV) 1, 2, 3 and 4 (A and B) cause approximately 39-40% of all acute respiratory infections in infants and children for which there is no effective therapy. Firstly, this thesis was aimed at ascertaining a suitable guinea pig model of PIV-3 infection by determining the most efficient route of virus application. Secondly, to ascertain if a temporal association may be established during the time course of infection (Day 1-40) by measuring the following parameters: body weight, rectal temperature, airway function (sGaw), airways reactivity to inhaled histamine, inflammatory cell infiltration to the lungs measured by bronchoalveolar lavage, wet lung weights, inflammatory markers (nitric oxide and total protein levels), lung histological analysis and recovery of the virus from bronchoalveolar lavage fluid and lung tissue. Further to this, experiments were also designed to determine the impact of the glucocorticoid, dexsamethasone (in vivo and in vitro) and the phosphodiesterase inhibitor, rolipram (in vivo). Lastly, this study ascertained the effect of pre-sensitisation with antigen on the responses of antigen in PIV-3 infected guinea pigs. These investigations have shown guinea pigs to be a suitable model for PIV-3 infection and intranasal inoculation is the most efficient route of virus application. In addition, these investigations also established a temporal association between the time course of PIV-3 infection including airway reactivity to histamine, airway function (sGBW), airways reactivity to inhaled histamine, inflammatory cell infiltration, wet lung weights, inflammatory markers (nitric oxide and total protein levels), pulmonary histopathology and recovery of the virus from bronchoalveolar lavage fluid and lung tissue. Pre-treatment of PIV-3 infected guinea pigs with the glucocorticoid, dexamethasone and the phosphodiesterase inhibitor, rolipram (in vitro) ameliorated the inflammatory response and airway hyperreactivity. Unlike rolipram, dexamethasone also reduced viral titre (in vivo and in vitro), supporting a role for the anti-viral effects of dexamethasone. The anti-inflammatory effects of dexamethasone are well known and it has been speculated by other authors which maybe caused by decreased viral receptors on the epithelial cells via inhibition of intracellular adhesion molecule-1 expression. Finally, in this study PTV-3 infection, enhanced the effect of pre-allergen sensitisation, which may arise from increased permeability of the airway mucosa to allergens, due to damage of the respiratory epithelium and increased recruitment of dendritic cells. In summary, this thesis has established a clearly defined efficacy of dexamethasone use in the treatment of PIV-3 infection.
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Tsuyuguchi, Kazunari. "Effect of estrogen on Mycobacterium avium complex pulmonary infection in mice." Kyoto University, 2001. http://hdl.handle.net/2433/150522.
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Lam, Phung Kim. "Factors associated with Mycobacterium avium complex infection and pulmonary disease progression /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2005. http://wwwlib.umi.com/cr/ucsd/fullcit?p3202827.
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Brandén, Eva. "Chronic infection with Chlamydia pneumoniae in COPD and lung cancer." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-344-2/.
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Hemann, Emily Ann. "Pulmonary dendritic cells and CD8 T cells facilitate protection following influenza A virus vaccination and infection." Diss., University of Iowa, 2014. https://ir.uiowa.edu/etd/1467.
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The severe disease associated with seasonal epidemics of influenza A virus (IAV), as well as pandemic outbreaks, have highlighted the necessity for novel, broadly cross-reactive vaccination and therapeutic strategies against IAV. Our studies have focused on the contribution of IAV-specific CD8 T cells to mediating protection following IAV vaccination and infection as IAV-specific CD8 T cells are required for clearance of IAV. Further, IAV-specific CD8 T cells are typically cross-protective as they are generally directed at highly conserved areas of IAV. Recently, influenza virus-like particles (VLPs) have been developed from recombinant baculoviruses containing influenza proteins hemagglutinin (HA) and/or neuraminidase (NA) on the surface and matrix (M1) in the VLP core. Influenza VLPs induce potent antibody responses and have been shown to provide protection from morbidity and mortality during lethal homo- and hetero-subtypic IAV challenge. This suggests that conserved, VLP-induced CD8 T cell responses may also contribute to the overall protective ability of VLPs. However, whether influenza VLPs can induce influenza-specific CD8 T cell responses and if these T cells are protective during IAV challenge remains unknown.
Here, I demonstrate that a single, intranasal vaccination with VLPs containing HA and M1 leads to a significant increase in HA533-specific CD8 T cells in the lungs and lung-draining lymph nodes. Our results also indicate that HA533-specific CD8 T cells primed by influenza VLP vaccination are significantly increased in the lungs following lethal IAV challenge. These VLP-induced memory CD8 T cells are critical in providing protection from lethality following subsequent challenge infections, as depletion of CD8 T cells leads to increased mortality, even when total, but not VLP-induced memory, CD8 T cell numbers have been allowed to recover prior to lethal dose IAV challenge. In addition, my studies also importantly demonstrate that these VLP-induced, HA533-specific CD8 T cells aid in protection from high-dose, heterosubtypic IAV infections where CD8 T cell epitopes are conserved, but the targets of neutralizing antibodies have been destroyed.
This dissertation further elucidates the requirements for the regulation of the IAV-specific CD8 T cell response in the periphery (i.e. lung) by pDC and CD8α+ DC. Our studies have previously demonstrated that pDC or CD8α+ DC must present viral antigen in the context of MHC class I along with trans-presentation of IL-15 to effector, IAV-specific CD8 T cells in the lungs to protect the T cells from apoptosis and allow generation of the full magnitude CD8 T cell response needed to clear IAV infection. Herein, I demonstrate that in addition to antigen presentation and IL-15, costimulatory molecules on the surface of pDC and CD8α+ DC are also required. However, the specific costimulatory molecules required depends upon both the mouse strain utilized for IAV infection as well as DC subset.
In addition to costimulatory molecules, I also demonstrate that the requirement for pDC and CD8α+ DC to be infected differs in order for them to participate in this pulmonary rescue of the IAV-specific CD8 T cell response. While CD8α+ DC are able to efficiently cross-present exogenous antigen, pDC must be directly infected and utilize the endogenous, direct antigen presentation pathway to present viral antigen to IAV-specific CD8 T cells in the lungs during IAV infection. These data suggest there are distinct differences between pDC and CD8α+ DC in their mechanism of regulating the pulmonary IAV-specific CD8 T cell response, which had not been previously appreciated.
Together, the results presented herein further detail the mechanism of regulation of effector IAV-specific CD8 T cells by DC as well as the contribution of IAV-specific CD8 T cells to a novel, IAV VLP vaccination strategy. These findings highlight the importance of IAV-specific CD8 T cells in mediating protection following IAV vaccination and infection.
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O'Shaughnessy, Blaze Georgia. "The role of platelets in the regulation of pulmonary infection and host defence." Thesis, King's College London (University of London), 2019. https://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-platelets-in-the-regulation-of-pulmonary-infection-and-host-defence(142a8b4b-cc16-4b02-b04e-82eef097f20a).html.
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Background. The implication of platelets in inflammatory disorders, such as asthma, has become increasingly more apparent. Following an inflammatory insult, platelets modulate inflammation by a number of distinct mechanisms, including pulmonary-leukocyte recruitment and release of platelet specific mediators. However, little is known regarding the role of platelets in the regulation of pulmonary infection. Pulmonary colonisation of bacteria, including Pseudomonas aeruginosa (P.aeruginosa) and Staphylococcus aureus (S.aureus) presents a therapeutic challenge due to antimicrobial resistance (AMR). Objectives. In this study, the effect of experimentally induced platelet depletion was investigated on infection and inflammatory parameters in a murine model of pulmonary infection. A new approach in targeting AMR was also tested, using a novel antibiotic enhancer compound, HT61. Methods. C57/B16 mice were experimentally depleted of platelets, 24 hours prior to infection with either sham, P.aeruginosa or S.aureus embedded agar beads. Bronchoalveolar lavage (BAL) fluid and lungs, kidney and spleen were analysed for inflammatory cells and bacterial load respectively. The role of platelet purinergic receptors was also assessed. In vitro assays were performed to investigate the effect of bacteria on platelet function, through measurements of platelet-leukocyte complexes and mediator release. Additional in vivo experiments were performed to test enhancer compound, HT61. Results. Infection induced pulmonary platelet recruitment (p < 0.01) in addition to a mild state of thrombocytopenia (p < 0.05). Evidence of platelet activation was detected in infected mice through increased levels of platelet-derived mediators Platelet Factor-4 (PF-4) and Regulated upon activation, normal T-cell expressed and secreted (RANTES) in BAL fluid and platelet-neutrophil complexes (p < 0.01) in blood. In mice depleted of circulating platelets, there was evidence of systemic bacterial dissemination and weight loss was increased compared to mice with normal platelet levels. Furthermore, pulmonary neutrophil recruitment was significantly reduced 24 hours post infection in mice depleted of circulating platelets. These results were reproduced following inhibition of the P2Y14 receptor and use of the ATP/ADP hydrolysing agent, Apyrase. HT61 as a singular treatment showed no inhibition of P.aeruginosa or S.aureus bacterial load, however, in combination with Tobramycin an enhanced reduction in bacterial load was observed for two strains of P.aeruginosa (p < 0.05) when compared to treatment with either drug alone. Conclusions. Here it is demonstrated that infection induces platelet activation and accumulation in the lungs. Mice depleted of circulating platelets or treated with Apyrase or a P2Y14 receptor antagonist demonstrated increased weight loss and increased systemic infection, this therefore suggests that in addition to the role played by neutrophils, platelets also have a distinct role in the host defence against bacterial infection. Furthermore, I demonstrated an enhancement of Tobramycin’s efficacy when administered in combination with HT61, highlighting a potential novel treatment to target AMR.
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Summers, Christina. "Immune responses during jaagsiekte sheep retrovirus infection and development of ovine pulmonary adenocarcinoma." Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/30805.
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Jaagsiekte sheep retrovirus (JSRV) is the aetiological agent of sheep pulmonary adenomatosis (SPA), a contagious bronchioloalveolar carcinoma, which imposes a serious economic burden on the sheep farming industry. This study evaluated the immunological responses during experimentally induced JSRV infection and tumorigenesis in conventionally housed and specific pathogen free (SPF) neonatal lambs, and in adult field cases in the terminal stages of SPA. This study identified, for the first time, changes in cellular function in the peripheral blood of JSRV-infected animals by measuring the in vitro lymphoproliferative response to various mitogens. The presence of JSRV did not affect the level of response to phytohaemagglutin (PHA) and pokeweed mitogen (PWM) stimulation, but a reduced response to concanavalin A (ConA) was demonstrated in the JSRV-infected animals. The reduced response to ConA was detected prior to the diagnosis of clinical symptoms and was also evident in the terminal stages of SPA. The presence of JSRV also affected the mitogenicity of the mannose-specific, monocotyledonous Narcissus pseudonarcissus lectin (NPA). The level of proliferation was comparable between JSRV-infected and control lambs, but post-stimulation phenotyping revealed an altered phenotypic profile, with elevated numbers of T and B lymphocytes from JSRV-infected animals. Furthermore, the addition of exogenous mannnose completely inhibited NPA mitogenicity in control but not in JSRV infected lambs. It has been established that NPA possesses insecticidal properties, which could potentially increase pest resistance in transgenic crops. During this study we revealed that NPA mitogenicity is age-dependent in sheep, with no lymphoproliferative response detected in adult animals. This research was extended to include human subjects, and we have shown that NPA is slightly mitogenic for adult lymphocytes but that mitogenicity is increased more than sevenfold for lymphocytes purified from umbilical cord blood. These findings indicate possible physiological implications as a result of introducing foreign lectins into human and animal food sources.
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Price, Brian M. "Studies on genetic immunization against Pseudomonas aeruginosa in a chronic pulmonary infection model /." The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu148657216527884.
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Geetha, Bharathi. "Screening for childhood pulmonary tuberculosis infection : a diagnostic strategy in a developing country /." Thesis, Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25101110.
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Ellis, Terri Noelle. "Interferon-gamma and innate immune responses to murine pulmonary infection with Nocardia asteroides /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2004. http://uclibs.org/PID/11984.
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Oliveira, Fernanda Paulina. "Análise do processo sinérgico da deglutição em pacientes portadores de bronquiectasia atendidos no Hospital Universitário Pedro Ernesto." Universidade do Estado do Rio de Janeiro, 2013. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=6039.
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A respiração e a deglutição são vitais para o homem. Enquanto a primeira diz respeito a um ato primitivo da vida, a hematose, a segunda trata da manutenção da vida, oferecendo a energia necessária, nutrindo e hidratando, perpassando pelo prazer alimentar, ato tão
importante na sociedade contemporânea. A relação funcional entre essas funções ainda não foi totalmente elucidada, porém é crescente o interesse e o número de estudos sobre esta temática. Considerando que a deglutição eficiente tem como pressuposto a capacidade de proteger via aérea inferior, a alteração de deglutição primária ou secundária a um dano pulmonar pode trazer repercussões severas para a integridade do sistema respiratório. O objetivo desse estudo é analisar o processo sinérgico da deglutição em portadores de
bronquiectasia, a fim de verificar se há alteração na fisiologia da deglutição e caracterizá-la, assim como, identificar se há correspondência entre alteração da função pulmonar e alteração da deglutição.Para tal foram selecionados randomicamente 30 pacientes na faixa etária de 18 a 65 anos, atendidos no ambulatório de bronquiectasia do HUPE. Destes, 26 indivíduos
responderam a um questionário dirigido sobre hábitos alimentares e possíveis dificuldades de alimentação; foram submetidos à avaliação clínica da deglutição; 22 fizeram espirometria no setor de prova de função pulmonar no HUPE e 17 avaliação videofluoroscópica da deglutição. Dos 26 indivíduos estudados 10 eram homens e 16 mulheres, com média de idade de 46,3
anos. Na avaliação clínica da deglutição observaram-se alterações estruturais e funcionais em todos os indivíduos estudados. As principais alterações estruturais detectadas referem-se e a dinâmica laríngea; enquanto na avaliação funcional detectou-se alterações referentes à ejeção oral, dinâmica hiolaríngea, trânsito faríngeo e presença de deglutições múltiplas. Com relação à espirometria 06 indivíduos apresentaram distúrbio obstrutivo leve; 04 distúrbio obstrutivo
moderado e 09 distúrbio obstrutivo acentuado. A videofluoroscopia da deglutição corroborou os achados da avaliação clínica da deglutição e evidenciou episódios de penetração e aspiração laríngea Pode-se concluir que: (1) a avaliação clínica da deglutição associada à
avaliação videofluoroscópica são métodos eficientes para a análise do processo sinérgico da deglutição; (2) identificou-se alteração do processo sinérgico da deglutição, nos indivíduos avaliados; (3) a ausculta cervical isoladamente, não demonstrou ser um método eficiente para predizer aspiração e/ou penetração laringotraqueal; (4) houve correspondência entre os
resultados da avaliação clínica funcional da deglutição e videofluoroscópica, exceto quanto a presença de penetração e/ou aspiração e quanto a capacidade de avaliar a ejeção oral; (5) não foi possível identificar se há correspondência entre alteração da função pulmonar e processo sinérgico da deglutição.Breathing, as well as swallowing, is vital to men.While the first accounts for a primitive aspect of life, the transference of gases through the blood-air barrier, the second is about the maintenance of life, supplying the necessary energy, nourishing and hydrating the organism and then touching the subject of feeding pleasure, such an important act in contemporary society. The functional relation between these functions has not been completely elucidated; however the interest is increasing and the number of studies about this theme. Considering that the efficient swallowing has the capacity of protecting the low airway as purpose, the alteration of primary or secondary swallowing to a pulmonary damage may bring severe repercussions to the integrity of the respiratory system. The aim of the study is to analyze the swallowing in patients carrying bronchiectasis, in order to verify whether there is an alteration in the swallowing physiology and characterize it, as well as to identify whether there is a correspondence between the alteration of the pulmonary function and swallowing disorders. 30 patients were randomly selected aged between 18 and 62 years old, attended at the bronchiectasis clinic of HUPE. 26 out of those individuals were evaluated. They answered a directed quiz about alimentary habits and possible alimentary difficulties; they were submitted to clinical evaluation of swallowing, 22 were orientated to spirometric evaluation in the sector of pulmonary function test at HUPE and 17 videofluorographic examination of swallowing. From the 26 individuals 10 were male and 16 were female, average age of 26 years old. As for the clinical evaluation of swallowing (structural and functional), all individuals presented some kind of laryngeal alteration in the structural evaluation. In the functional evaluation was noted that the main alterations referred to oral ejection, elevation and anterior movement of the hyoid and larynx, pharyngeal transit and multiple swallowing were also present. In relation to spirometry 06 individuals presented mild obstructive disorder 04 presented moderate obstructive disorders and 09 presented severe obstructive disorders. The videofluorograph examination confirmed the findings of the swallowing clinical evaluation and made clear an episode of larynx penetration of liquids. The present study showed as preliminary results: (1) that the clinical evaluation of swallowing associated with videofluorographic Examination are efficient methods to the analysis of the swallowing process; (2) Alteration in the synergic process of swallowing was identified in the evaluated individuals; (3) Cervical auscutating isolatedly did not prove to be an efficient method to predict larynx-tracheal aspiration and/or penetration; (4) There was a correspondence between the results of clinical evaluation of the swallowing videofluorographic, except for the presence of penetration and/or aspiration and for the capacity of evaluating oral ejection; (5) Was not possible to identify if there is a correlation between alteration of the pulmonary function and swallowing disorders.
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Poux, Candice Maria Yvette. "Characterization of pulmonary langerin-expressing dendritic cells in a model of respiratory viral infection." Thesis, Queen's University Belfast, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.557838.
Full textAbstract:
Understanding the control of pulmonary dendritic cells (DC) function during respiratory virus infection may lead to novel prophylactic and antiviral therapeutic strategies, Three subsets have already been identified: plasmacytoid DC (pDCL eerie DC and CD103+ DC which express the C-type lectin langerin. To further characterize the different pulmonary DC, experiments were undertaken in transgenic eGFP/DTR F1 mice, in which all langerin-expressing cells express eGFP and human diphtheria toxin receptor (DTRL) offering the unique possibility to address the role of CD103+ DC, , both during homeostatic and inflammation states. Interestingly, immunophenotyping of pulmonary DC from these mice demonstrated that not all CD103+ DC are tang", but both subsets exhibited an immature phenotype in the lung and mature upon arrival in the mediastinal lymph node (mLNL) suggesting the possibility of immune redundancy. Sendai virus (SeVL) a mouse parainfluenza virus, causes acute viral inflammation of the small airways that is comparable to viral bronchiolitis in humans, We generated a recombinant SeV that expresses a red fluorescent protein/ovalbumin fusion protein (SeV-OVATdT), It was designed to help tracking viral infection in vivo and to perform functional studies addressing the role of pulmonary DC during respiratory virus infection. At 5 days post-infection, SeV-OVATdT induced bronchiolitis and interstitial pneumonia equivalent to SeV WT infection, and significant changes in pulmonary DC populations compared to mock-infected controls. Specifically, all DC characterized here increased in SUMMARY 1 - PAGE 2 significantly more inflammatory DC and CD8a+ DC were found in mLN, while number of pulmonary pDC was maintained. Additionally, viral replication was restrained and significantly more SeV- specific CD8+ T cells were recruited to lungs. Altogether, these results indicate that pulmonary CD103+ l.ang" DC negatively modulate antiviral immune responses.
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Singanayagam, Aran. "Effect of inhaled corticosteroids on viral and bacterial infection in chronic obstructive pulmonary disease." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/24469.
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Rhinovirus (RV) infections trigger exacerbations of chronic obstructive pulmonary disease (COPD) exacerbations and may precipitate secondary bacterial infections. Inhaled corticosteroids (ICS) are used commonly in COPD but are relatively ineffective in the context of virus-induced exacerbations and may also increase the risk of pneumonia. We hypothesised that, in a mouse model, ICS would suppress anti-viral and anti-bacterial immune responses leading to alteration of the airway microbiota and secondary bacterial infection following RV-induced exacerbation of COPD. Despite extensive optimisation, we were unable to define a representative mouse model of the deficient anti-viral and anti-bacterial responses that are indicative of human COPD. For this reason, and because of difficulties in measuring the airway microbiota in mice, we employed models of primary RV1B and Streptococcus pneumoniae infection as surrogates for viral exacerbation and bacterial colonisation in COPD. Fluticasone propionate (FP) administration prior to RV1B infection suppressed innate and adaptive immune responses leading to impaired virus control, in a dose dependent manner. This effect was causally related to suppression of type I interferon (IFN) as administration of recombinant IFN-β reconstituted IFN-stimulated gene expression and restored virus control. FP suppressed RV-induced airway inflammation but led to enhanced airway mucin production, effects that were unaltered by recombinant IFN-γ. FP administration also suppressed innate responses to S. pneumoniae including expression of anti-bacterial cytokines and cathelicidin-related anti-microbial peptide. High dose FP increased lung tissue bacterial loads with the opposite effect observed with lower dose FP despite similar anti-inflammatory effects. Our findings demonstrate beneficial anti-inflammatory effects of ICS during virus-induced COPD exacerbations but reveal some previously unrecognised detrimental effects including increased virus replication and enhanced mucin production. Additionally, we show that high dose ICS administration may increase bacterial loads and thus increase pneumonia risk but lower doses may conversely reduce bacterial loads and therefore could be safer in COPD.
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Maung, Nang H. "Intranasal Colonization by Streptococcus Pneumoniae Induces Immunological Protection from Pulmonary and Systemic Infection: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/570.
Full textAbstract:
Given that Streptococcus pneumoniae can cause life-threatening pulmonary and systemic infection, an apparent paradox is that the bacterium resides, usually harmlessly, in the nasopharynx of many people. Humoral immunity is thought to be the primary defense against serious pneumococcal infection, and we hypothesized that nasopharyngeal colonization of mice results in the generation of an antibody response that provides long-term protection against lung infection. We found that survival of of C57L/6 mice after intranasal inoculation with wild-type serotype 4 strain TIGR4 pneumococci required B cells but not T cells, suggesting that nasopharyngeal colonization elicited a protective humoral immune response. In fact, intranasal inoculation resulted in detectable pneumococcal-specific antibody responses, and protected mice against a subsequent high-dose S. pneumoniae pulmonary challenge. B cells were required for this response, and transfer of immune sera from i.n. colonized mice, or monoclonal antibodies against phosphorylcholine, a common surface antigen of S. pneumoniae, was sufficient to confer protection. IgA, which is thought to participate in mucosal immunity, contributed to but was not absolutely required for protection from pulmonary challenge. Protection induced by i.n. colonization lasted at least ten weeks. Although it was partially dependent on T cells, depletion of CD4+ T cells at the time of challenge did not alter protection, suggesting that T cells did not provide essential help in activation of conventional memory cells. Peritoneal B1b cells and radiation-resistant, long-lived antibody secreting cells have previously been shown to secrete anti-pneumococcal antibodies and mediate protection against systemic infection following immunization with killed bacteria or capsular polysaccharide [1, 2]. We found that peritoneal cells were not sufficient for colonization-induced protection, but sub-lethally irradiated mice largely survived pulmonary challenge. Thus, our results are consistent with the hypothesis that nasopharyngeal colonization, a common occurrence in humans, is capable of eliciting extended protection against invasive pneumococcal disease by generating long-lived antibody-secreting cells.
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Alhariri, Moayad Abdulaziz I. "EVALUATION OF LIPOSOMAL BISMUTH-ETHANEDITHIOL-TOBRAMYCIN FOR TREATMENT OF CYSTIC FIBROSIS PULMONARY PSEUDOMONAS AERUGINOSA INFECTION." Thesis, Laurentian University of Sudbury, 2013. https://zone.biblio.laurentian.ca/dspace/handle/10219/2099.
Full textAbstract:
The effectiveness of liposomes incorporating bismuth-ethanedithiol and loaded with tobramycin (LipoBiEDT-TOB) at sub-inhibitory concentrations to inhibit the production of quorum sensing signaling molecules and virulence factors induced by P. aeruginosa was evaluated in vitro. In addition, we evaluated the efficacy and safety of free and encapsulated tobramycin in liposomal formulations administered intratracheally to rats chronically infected with P. aeruginosa. LipoBiEDT-TOB significantly reduced the production of quorum sensing signaling molecules and virulence factor secretion compared to free tobramycin. The LipoBiEDT-TOB formulation significantly reduced the bacterial count in lungs, modulated the IL-8 level in blood and minimized the nephrotoxicity that is associated with aminoglycoside treatment. These results support the hypothesis that aerosolization of liposomal aminoglycosides may enhance the management of chronic lung infections caused by resistant P. aeruginosa in patients with cystic fibrosis.
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Kerr, Margaret Heather. "An investigation of the pulmonary surfactant system in children with severe respiratory syncytial virus infection." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265640.
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Crossley, Brian E. "Role of the Exopolysaccharide Alginate in Adherence to and Inflammation of Pulmonary Epithelial Cells." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4473.
Full textAbstract:
Pseudomonas aeruginosa (PA) infections in Cystic Fibrosis (CF) patients are not easily cleared due to the conversion from a nonmucoid to a mucoid phenotype. Alginate is an acetylated exopolysaccharide produced by mucoid PA that is responsible for increased resistance to antibiotics, host phagocytic killing, and propagating biofilm formation. Understanding the interaction between PA and host cells is critical to understanding chronic infection and inflammation in CF. In order to investigate this, we used A549 pulmonary epithelial cells and murine alveolar macrophages (MH-S) to examine host response to nonmucoid versus mucoid PA infection. Adhesion assays in A549 pulmonary epithelial cells revealed that mucoid PA mutants adhere poorly compared to their nonmucoid counterparts. Similarly, phagocytosis assays using MH-S infected with PA revealed that mucoid PA are increasingly resistant to phagocytosis. The alginate acetylation mutant FRD1175 is more susceptible to phagocytic killing than alginate+ FRD1. Adherence and phagocytosis of mucoid FRD1 was increased by increasing the multiplicity of infection (MOI) from 50:1 to 500:1. Furthermore, confocal microscopy revealed that mucoid PA are inherently less inflammatory than nonmucoid strains in both A549 and MH-S. Increasing the MOI of mucoid FRD1 from 50:1 to 500:1 significantly increased caspase-1 activation in MH-S but not in A549, revealing that intensity of inflammatory signaling by epithelial cells is likely independent of increased adherence. FRD1175 infection in both A549 and MH-S revealed that alginate acetylation plays a significant role in reducing inflammasome activation. Western analysis revealed that PA does not actively induce TGF-β secretion by A549 epithelial cells. Similarly, NF-κB expression was reduced in both A549 and MH-S when infected with mucoid FRD strains, but not PA from the PAO background, suggesting FRD strains have accumulated additional mutations facilitating escape of inflammation. MH-S treated with cytochalasin D to block phagocytosis were still able to activate NF-κB signaling, suggesting NF-κB activation is adherence but not phagocytosis dependent. These data increase our understanding of the various mechanisms in which mucoid PA is able to evade host immune defenses and provides insight into potential therapies to treat PA infections.
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Dhar, Jayeeta. "Suppression of Pulmonary Innate Immunity by Pneumoviruses." Cleveland State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=csu1479673989904175.
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Liu, Huan. "Discover the Role of Dendritic Cell in Pulmonary Langerhans Cell Histiocytosis And Respiratory Syncytial Virus Infection." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1535382725511759.
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Seddigh, Pegah [Verfasser], and Matthias [Akademischer Betreuer] Gunzer. "Characterization of the murine pulmonary phagocytic network during Aspergillus fumigatus infection / Pegah Seddigh ; Betreuer: Matthias Gunzer." Duisburg, 2017. http://d-nb.info/1141053578/34.
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Bayes, Hannah Kelly. "The production and function of IL-17A and IL-22 in chronic pulmonary Pseudomonas aeruginosa infection." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5403/.
Full textAbstract:
Cystic fibrosis (CF) lung disease typically results in pulmonary infections and inflammation that produces progressive respiratory failure. The most common pathogen in adult patients with CF is Pseudomonas aeruginosa (PA), which in the majority of patients chronically colonises the airways and is associated with a neutrophil-dominated host response. This neutrophilic response fails to clear the infection but contributes to progressive lung injury. Prior to the establishment of chronic PA colonisation, patients experience intermittent pulmonary PA infections that can be cleared either by host responses or antibiotic eradication therapy. Recent attention has focused on the role of the cytokines interleukin-17 (IL-17) produced by T helper 17 (Th17) cells, in anti-microbial defences. IL-17 plays a critical role in the generation and recruitment of neutrophils to sites of infection and has been implicated in responses to PA as well as other pulmonary pathogens. Clinical data has also suggested a potential role for IL-17, Th17 cells, as well as other cellular sources of IL-17 in the pathogenesis of human CF pulmonary disease. An additional Th17-related cytokine IL-22 has previously been shown to hold a critical role in defence against acute pulmonary infections, as well as reparative functions in pulmonary disease. However, the functions of this cytokine are not clear cut, since pro-inflammatory effects are also seen depending on the local environment in which it acts. Given the pivotal role of IL-17 in neutrophilic immune responses, in this thesis I hypothesised that IL-17A is beneficial in early CF lung disease where it aids clearance of PA and delays the onset of chronic PA colonisation. However, as the organism adapts to the hostile environment and/or the lung environment becomes more conducive to bacterial growth then chronic PA infection inevitably develops; in this setting I proposed that IL-17A becomes pathogenic by driving persistent, damaging neutrophilic inflammation. In addition, I hypothesised that Th17 cells are a source of IL-17A in PA infection and that, due to persistent antigenic-stimulation in CF patients the Th17 response may be altered to that seen in healthy controls. I further proposed that IL-22 may have a reparative and protective role in persistent pulmonary PA infection, but that the cytokine's reparative effects become overwhelmed or IL-22 becomes pro-inflammatory and pathogenic in later CF lung disease with chronic PA colonisation. These hypotheses were addressed via the use of both clinical samples from patients with CF and a murine model of persistent PA infection.
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Foxwell, Alice Ruth, and n/a. "Mechanisms of immunity to nontypeable Haemophilus influenzae in the lung." University of Canberra. Applied Science, 1998. http://erl.canberra.edu.au./public/adt-AUC20060710.142114.
Full textAbstract:
Pulmonary infection caused by nontypeable Haemophilus influenzae (NTHi) is a
significant cause of morbidity and mortality in both industrialised and developing
countries. Previous work from this group resulted in the development of a respiratory
model in rodents which has precipitated studies into the pathogenesis of infection by
NTHi and investigation of the humoral and cellular mechanisms by which the bacteria
are cleared from the lung. Comparison of mucosally immunised with non-immunised
animals has demonstrated that not only are bacteria cleared more rapidly from the lungs,
but there is a more rapid response and resolution of inflammatory factors in the
mucosally immunised animals following challenge with NTHi.
This inflammatory response is partially regulated by the ability of the mucosally
immunised animals to rapidly produce, then control the production of tumour necrosis
factor (TNF)-a. The TNF-a is produced by both macrophages and type I pneumocytes
in the alveoli and also by the endothelial cells lining the blood vessels in the lungs.
Immunocytochemical studies have identified cellular subsets accumulating in the lung
at various time points following infection. Marked differences in cellular infiltration
into the lung tissue were noted between immunised and non-immunised animals after
challenge with NTHi. Immunised animals demonstrated an early influx of
macrophages, CD8+ T cells and Y8+ T cells, followed by enhanced expression of the
MHC-II marker, cellular infiltration by polymorphonuclear leukocytes and finally an
increased number of both B cells and CD4+ T cells. In contrast, non-immunised
animals did not demonstrate any proliferation nor extravasation of lymphocytes or
increased expression of MHC-II before total bacterial clearance had occurred.
Polymorphonuclear leukocyte infiltration occurred in the non-immunised animals,
however at a later time than that seen in immunised animals.
Challenging rodents to establish persistent infection highlighted the inappropriately
aggressive white blood cell response to an initial challenge when bacteria may be
masked by other substances, followed by the inability to amplify the
polymorphonuclear leukocyte response on repeated challenge with NTHi. This
hyporesponsiveness in the macrophage population, shown by lack of detectable TNF-a
production, concomitant with low numbers of NTHi resulted in a continuously high
number of macrophages in the alveoli and the possibility of increased damage to the
lung tissue.
The requirement for cell surface TNF-a and CD8+ T cells to enhance the clearance of
NTHi from the lungs further strengthens previous in vitro and in vivo findings of the
possible significance of cellular invasion as a mechanism of pathogenicity for NTHi.
This thesis has contributed to the understanding of both the immune response to and the
pathogenicity mechanisms of pulmonary infection with NTHi. Kinetic studies
identifying cellular responses and cytokine levels have emphasised the ability of
mucosal immunisation to increase the rate of immune response and resolution of
inflammation to NTHi infection in the lung. Observations demonstrating a requirement
for macrophages and CD8+ T cells in mechanisms associated with enhancing NTHi
clearance from the lung will lead to further investigations.
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Sivell, Michael. "Cryptococcosis: a proteomic investigation of an emerging fungal disease." Thesis, The University of Sydney, 2013. http://hdl.handle.net/2123/10185.
Full textAbstract:
Fungal infections are increasing in frequency throughout the world. The development of new diagnostic and treatment strategies has not kept pace with this increase. The result is a high incidence of infection recurrence and high mortality rates. The pathogenic yeasts Cryptococcus neoformans and Cryptococcus gattii provide an excellent system for determining the spectrum of fungal growth and infection, from environmental saprotrophic growth, to self-limiting infection and through to severe primary infection. Cryptococcus cells obtained from pulmonary infection, and infected rat lung tissue, represented technically challenging sample types that required significant protocol development prior to comparative analysis. This subjected the obtained data to a number of experimental caveats. Despite the significant impediments to experimentation, the advances made in protocol development by this study allowed for the first in vivo analysis of intracellular Cryptococcus protein expression. This result provided proof of concept for global "–omics" analysis of Cryptococcus from an in vivo sample. In addition, qualitative data were obtained that offered insights into fungal pathogenesis at the protein level and highlighted a number of Cryptococcus proteins that could be exploited as drug targets. Furthermore, the identification of host lung proteins and systemic cytokines of biological relevance to pulmonary cryptococcosis provides proof of the ability of comparative proteomics to elucidate future drug targets, biomarkers and diagnostic markers from in vivo mammalian infection models. The studies’ most significant achievement has been the advances made in protocol development. It is hoped that these advances will lead to further, potentially quantitative, analysis of fungal pathogens under in vivo conditions, along with continued development of novel therapeutic and diagnostic options for pathogenic fungi.
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Leja, Astrid. "The lectin-like TNF domain role in experimental models of pulmonary edema reabsorption and Trypanosoma brucei infection /." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=97288128X.
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Anis, Mursalin M. "Modulation of naive CD4+ Tcell activation and dendritic cell function in the lungs during pulmonary mycobacterial infection." Connect to text online, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1184427168.
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Shead, Elizabeth F. "Cystic fibrosis related osteoporosis : does the systemic inflammatory response to pulmonary infection influence osteoclast formation and activity?" Thesis, University of Bristol, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441335.
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Whitacre, Brynne E. "Restoration of Lung Sphingosine Levels Improves the Immune Response to Infection in a Murine Two-hit Sepsis/Pneumonia Model." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1504794762765183.
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Nurbaeti, Siti Nani. "Études biopharmaceutiques et formulation de chloramphénicol et de thiamphénicol pour le traitement ciblé des infections pulmonaires par voie inhalée." Thesis, Poitiers, 2017. http://www.theses.fr/2017POIT1802/document.
Full textAbstract:
L'émergence rapide de bactéries résistantes et l’absence de nouveaux traitements efficaces ont conduit à réutiliser d’anciens antibiotiques. Le chloramphenicol (CHL) et le thiamphenicol (THA) ont ainsi été proposés pour traiter les infections respiratoires multirésistantes. Leur administration directe dans les poumons sous forme d’aérosols thérapeutiques devrait augmenter leur efficacité et minimiser l’exposition systémique responsable d’effets secondaires, en particulier lors de traitements prolongés. Ce travail de thèse a eu pour objectifs de réaliser des étudies biopharmaceutiques et de développer des formulations d’aérosols pour la voie pulmonaire. La perméabilité membranaire du CHL et du THA a été évaluée sur le modèle d’épithélium bronchique Calu-3 et leur pharmacocinétique a été réalisée chez le rat après administrations intratrachéale et intraveineuse. La perméabilité membranaire in vitro du CHL s’est révélée élevée, et intermédiaire pour le THA. Les deux antibiotiques sont substrats de transporteurs membranaires d’efflux. Les études pharmacocinétiques, cohérents avec les études in vitro, ont montré un impact nul de la voie d’administration dans cas du CHL et modéré dans le cas du THA. Par conséquent, pour prolonger l’exposition pulmonaire à ces antibiotiques, des formulations à libération prolongées basées sur des nanoparticules ont été incluses dans des poudres sèches de microsphères pour inhalation. Ces poudres se caractérisent par une teneur optimale, des propriétés aérodynamiques satisfaisantes et un profil de libération prolongée, et sont donc prometteuses pour l’administration pulmonaire de CHL ou de THA sous la forme d’aérosolsThe rapid emergence of resistant bacteria and the lack of new efficient treatments lead to re-use old forgotten, but still effective, antimicrobials. In particular, chloramphenicol (CHL) and thiamphenicol (THA) have been proposed to treat multidrug-resistant pulmonary bacterial infections. Their direct administration into the lungs as therapeutic aerosols should increase their efficiency and minimize whole body exposure responsible for adverse effects, particularly in the case of prolonged treatments. The purpose of these PhD. works was to perform biopharmaceutical studies and to develop an effective aerosol formulation for lung delivery. The membrane permeability of CHL and THA was evaluated in vitro in the Calu-3 bronchial epithelial cell model and pharmacokinetic (PK) studies were carried out in rats after intratracheal and intravenous administration. In vitro membrane permeability of CHL was high, but intermediate for THA. Both compounds were shown to be substrates of membrane efflux transporters. In agreement with these findings, the PK studies showed that the administration route had no impact in the case of CHL and a moderate one in the case of THA. Therefore, in order to prolong lung exposure to CHL and THA, nanoparticle-based formulations with sustained release properties were formulated using the palmitate ester prodrugs of CHL and THA. To ease administration, nanoparticles were included in microsphere-based dry powder for inhalation. These powders showed an optimal content, satisfactory aerodynamic properties and sustained drug release, which make them promising formulations for lung delivery of CHL and THA as aerosols
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Fuchs, Stephan [Verfasser]. "Validierung des Clinical Pulmonary Infection Score bei intensivmedizinischen Patienten mit Pneumonie unter Berücksichtigung von Gender Aspekten / Stephan Fuchs." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/1202044905/34.
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Anis, Mursalin M. "MODULATION OF NAIVE CD4+ T CELL ACTIVATION AND DENDRITIC CELL FUNCTION IN THE LUNGS DURING PULMONARY MYCOBACTERIAL INFECTION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=case1184427168.
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Weisner, Abbie Michelle. "Development of rapid tools for the early diagnosis of Pseudomonas aeruginosa pulmonary infection in patients with cystic fibrosis." Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/11956.
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Pseudomonas aernginosa causes chronic lung infections in patients with cystic fibrosis (CF) and is associated with a marked decline in clinical status. Early detection ofthe organism and aggressive specific antibiotic treatment is beneficial to the patient and delays the onset ofchronic infection. The detection ofserum antibodies to P. aernginosa has been reported utilising a wide range ofantigens. The first part ofthis study used SDS-PAGE and immunoblotting to investigate protein and lipopolysaccharide (LPS) antigens from reference and clinical strains and the CF senun antibody response to them. The A-band LPS species, which was not serotype-specific, was studied further and its prevalence determined. It was found to be highly specific for P. aeruginosa, common to approximately 90 % ofclinical strains tested and provoked a strong antibody response. Serum and non-invasive samples (oral fluid, sputum and urine) from CF patients, patients with primary ciliary dyskinesia and healthy volunteers were analysed for A-band LPS-specific antibodies using SDS-PAGE and immunoblotting. Both oral fluid and sputwu showed excellent correlation with senun for antibodies to A-band. Since Pseudomonas-specific antibodies were found in healthy volunteer samples, it was necessary to develop a quantitative ELISA. Both IgM and IgG-specific assays were optimised. The serwn antibody response was further assessed by comparison to culture ofP. aernginosa from sputum, conversion ofP. aernginosa to the mucoid phenotype and lung function data. The IgG-specific assay clearly distinguished clinical infection, although no patients were shown to seroconvert prior to growth ofthe organism from sputum. IgM-specific antibody levels were significantly associated with positive sputum culture, in 83 % ofpatients. Finally, the IgG-specific assay was compared to the current in-house ELISA and two commercial products. There was moderate correlation between the developed assay, the in-house assay and one ofthe commercial kits.
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Lambert, Laura. "Immunology of the neonatal lung and the long term consequences of neonatal respiratory virus infection for pulmonary innate immunity." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/55261.
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Early life is a period of increased vulnerability to infection, particularly of the respiratory tract. The neonatal adaptive immune system is immature, with a bias towards Th2/Th17 responses and against Th1. Very little is understood about the innate response in early life, especially at mucosal surfaces such as the lung. To address this, Toll-like receptor (TLR) ligands were administered intranasally to neonatal and adult mice. In neonates, pulmonary neutrophilic influx was barely detectable, and expression of inflammatory chemokines greatly attenuated. Administration of exogenous CXCL1 elicited a strong neutrophilic response, indicating that diminished chemokine production is a limiting factor for cellular inflammation in early life. An unbiased microarray approach revealed that whilst expression of immune-related genes was mostly suppressed in the naïve neonatal lung, antimicrobial peptides such as cathelicidin were over-expressed. These novel findings challenge the perception that the infant immune system is simply an ‘immature’ version of the adult system, with implications for development of vaccines and adjuvants for this vulnerable population. An important respiratory pathogen of infants is respiratory syncytial virus (RSV), which can cause bronchiolitis, and in clinical studies is linked with lung dysfunction such as asthma and wheezing later in life. However, the mechanisms by which early life RSV infection could cause these delayed sequelae are unknown, and the effect on the innate immune response has not been explored. The long-term consequences of early life RSV infection were investigated using a murine model. Following neonatal RSV infection, allergen challenge resulted in an exaggerated inflammatory response in the adult murine lung, indicating that pulmonary innate immunity was dysregulated. Further, expression of various immune response, apoptosis-related and circadian rhythm genes was found to be altered. These data provide new evidence that infantile RSV has a causative effect on later lung dysfunction and identify gene targets for further investigation.
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Moore, Brian David. "Characterization of the pathogenesis of equine arteritis virus infection of cultured equine mononuclear phagocytes and pulmonary artery endothelial cells /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2003. http://uclibs.org/PID/11984.
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Sawtell, Amy. "Investigating neutrophil phenotype and migration mechanisms in the tissue draining lymph node during acute pulmonary infection with Streptococcus pneumoniae." Thesis, University of York, 2015. http://etheses.whiterose.ac.uk/8896/.
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Neutrophils are innate immune cells that form part of the first line of defense against pathogens. These cells are rapidly mobilised in response to infection and inflammation and are equipped with a range of pathogen destruction mechanisms. In recent years it has been demonstrated that neutrophils can also modulate innate and adaptive immune responses. Neutrophils have been found to enter secondary lymphoid organs including lymph nodes, however the phenotype and function of neutrophils in lymph nodes is not well understood. Work in this thesis utilised an acute pulmonary infection model with the lung pathogen Streptococcus pneumoniae, to investigate neutrophil recruitment, phenotype and function in the lung draining (mediastinal) lymph node. It was hypothesised that neutrophil phenotype and behaviours are not cell intrinsic, rather dictated by the localised microenvironment of the cell. To investigate this hypothesis a combination of flow cytometry, immunohistochemistry, quantitative PCR and four dimensional multiphoton explant imaging was used. Neutrophil recruitment to the lung draining lymph node was rapid, peaking at 6 - 12 hours post infection. Neutrophils were localised in the lymphatic sinus, specifically in areas with medullary macrophages. Neutrophil migration in this region was highly dynamic, with swarms of neutrophils observed. When compared to blood, lung and airway neutrophils, lymph node neutrophils showed an intermediate activation profile, similar to lung tissue neutrophils. Interestingly a small population of lymph node neutrophils expressed markers of antigen presenting cells. Neutrophils in the lymph node utilised mainly chemotactic migration mechanisms involving phosphatidylinositde 3-kinase signalling and leukotriene B4, however migration was not completely integrin independent. Thus the results support the hypothesis that neutrophil phenotype and behaviours are environment dependent as opposed to cell-intrinsic, also they demonstrate and support the evolving view of the neutrophil as a complex cell type that has multiple functional profiles and mechanisms of migration.
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McGill, Jodi Lynn. "The role of pulmonary dendritic cells in regulating the antigen-specific CD8 T cell response following influenza virus infection." Diss., University of Iowa, 2010. https://ir.uiowa.edu/etd/549.
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We have recently demonstrated in a model of influenza A virus (IAV) infection that the absence of specific pulmonary DC subsets, including plasmacytoid DC (pDC) and CD8a+ DC, from the lungs leads to a significant decrease in the number of virus-specific CD8 T cells. Reconstitution of the lungs with physiologic numbers of pDC or CD8a+ DC is able to restore the pulmonary IAV-specific CD8 T cell response to near normal levels via a mechanism that is dependent upon direct DC:T cell interactions, DC-expressed MHC I and the presence of viral antigen. Interestingly, however, this rescue is DC subset specific, as reconstitution with purified alveolar and airway DC or alveolar macrophages was unable to rescue the virus-specific CD8 T cell response. Following IAV infection there is an abundance of IAV antigen and MHC I expressing cells present in the lungs, including infected epithelial cells. Given this fact and the inability of all DC subsets to rescue the virus-specific CD8 T cell response, it suggested that there were additional, undefined requirements for pDC- and CD8a+ DC-mediated rescue of the T cell response in the lungs. Further, although it was known that the reduction in virus-specific CD8 T cells in the lungs was a result of increased T cell apoptosis, it remained unclear what pathways of apoptosis were contributing to the increased cell death, and what mechanism pulmonary DC subsets were utilizing to rescue this defect.
Here, we demonstrate that in the absence of lung-resident DC subsets, virus-specific CD8 T cells undergo significantly increased levels of apoptosis via both extrinsic activation induced cell death and intrinsic activated cell-autonomous death pathways. Reconstitution of aDC depleted lungs with pulmonary pDC and CD8a+ DC promotes increased T cell expression of the pro-survival molecule Bcl-2 and hence, increased T cell survival and accumulation in the lungs. Our studies herein demonstrate that pulmonary DC subsets utilize a variety of mechanisms to promote the rescue of virus-specific CD8 T cells in the lungs. Blockade of the costimulatory molecules CD70, and in some cases, 4-1BBL and OX40L, ablates the pulmonary DC mediated rescue of CD8 T cell numbers in the lungs, suggesting that late costimulation is one essential mechanism that pulmonary DC use to regulate CD8 T cell immunity following IAV infection. Further, we demonstrate that the absence of DC following IAV infection results in significantly reduced levels of IL-15 in the lungs and that pulmonary DC-mediated rescue of virus-specific CD8 T cell responses in the lungs requires the trans-presentation of IL-15 via DC-expressed IL-15Ra. In addition to the role of pulmonary DC mediated costimulation and IL-15 trans-presentation, we further demonstrate a previously unrecognized role for viral antigen in regulating the accumulation of both pulmonary DC and virus-specific CD8 T cells in the lungs, suggesting that viral load can dictate the nature of the inflammatory environment in the lungs and thus, regulate the character of the ensuing IAV-specific immune response.
Collectively, the results detailed here demonstrate a previously unrecognized role for pulmonary DC in regulating primary IAV-specific CD8 T cell immunity, and hence, promoting enhanced viral clearance and recovery from disease.
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Anderson, Beth Naomi. "The effects of an upper respiratory infection on resting pulmonary function and physiological responses during graded exercise in young adults." Virtual Press, 1994. http://liblink.bsu.edu/uhtbin/catkey/902472.
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Viral illnesses are the most common agents affecting humans. Due to their widespread affects, viruses may have a particular influence on exercise functional capacity. Therefore, the purpose of this study was to determine the impact of an Upper Respiratory Infection (URI) on exercise functional capacity, as measured by VO2max. In addition, submaximal exercise responses, changes in resting pulmonary function, the impact of select symptoms, and level of initial fitness on performance during an URI were also determined. Forty-five subjects (females=21, male=24) between 18 and 29 years of age participated in this study and were assigned to a mild or severe illness group based on symptom severity. There was also a control group of 10 subjects (female=5, male=5). An initial serological screening was performed on all experimental subjects to assess for the RV16 antibody.Subjects testing negative for the antibody performed a baseline graded exercise test to volitional fatigue, as well as pulmonary function tests. Each subject was inoculated two consecutive days with the RV16 virus within ten days of the baseline exercise test. The day following the second inoculation (peak illness) the subjects performed post-pulmonary function and exercise tests. The control subjects performed two resting pulmonary function and exercise tests separated by one week. Significance was set at p<0.05. Repeated measures ANOVA revealed a significant interaction in V02 at submaximal and maximal levels between trials for all groups (p<0.045). A significant interaction for VE for all levels and all groups was found (p<0.002). No impairment in resting pulmonary function was observed. Analyses of symptoms, and initial V02 in regard to performance, also revealed no significant differences. Therefore, the results seem to indicate that an URI does not limit one's ability to perform at submaximal or maximal levels of exercise, however, some relationship seems to exist. Further research is needed to clarify the effects of an URI on physical performance.School of Physical Education
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Neff-Laford, Haley D. "Examining dioxin-mediated alterations in pulmonary immune cell function during influenza virus infection : effects on cytolytic activity and interferon gamma." Online access for everyone, 2006. http://www.dissertations.wsu.edu/Dissertations/Spring2006/H%5FNeff-LaFord%5F050306.pdf.
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Van, Epps Heather Lin. "Long-Lived Memory T Lymphocyte Responses Following Hantavirus Infection: a Dissertation." eScholarship@UMMS, 2001. https://escholarship.umassmed.edu/gsbs_diss/112.
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Hantaviruses are members of the virus family Bunyaviridaethat cause two potentially life-threatening diseases in humans: hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (BPS). HFRS is caused by Old World hantaviruses that are endemic in many Asian and European countries. Infections with Old World hantaviruses can range in severity from asymptomatic to moderate or severe, depending primarily on the infecting serotype of virus. HPS is caused by New World hantaviruses in North and South America. New World hantaviruses are rarely asymptomatic and are severe in the majority of cases. These syndromes are distinct from one another in the primary target organ of virus infection (kidney vs. lung), but have important clinical features in common, including fever, thrombocytopenia, and a capillary leak syndrome. These common clinical manifestations suggest that the underlying mechanisms of disease may be similar in the two syndromes.
The precise mechanisms of pathogenesis of HFRS and HPS are poorly characterized, but may be mediated in part by immunopathology. Hantaviruses are able to establish infections in many human cell types, including primary human endothelial cells, without having any cytopathic effect on these cells. Human infections with hantavirus result in a robust activation of the humoral and cellular immune response, and we hypothesize that these immune responses contribute to the pathology of disease. Evidence for the activation of T lymphocytes, and their potential involvement in immunopathology, includes increases in the number of circulating, activated CD8+ T cells during HFRS, the presence of lymphocytic infiltrates (predominantly CD8+T cells) in kidney biopsies from patients with acute HFRS, and associations between certain HLA haplotype and disease severity following hantavirus infection. This thesis is the first examination of human T lymphocyte responses that are generated during HFRS. Initially, we studied memory T cell responses in scientists who were sub-clinically infected with Hantaan virus (HTNV), the prototype hantavirus. We later investigated memory T cell responses in healthy Finnish adults who had HFRS caused by Puumala virus (PUUV), a hantavirus endemic primarily in Scandinavia.
At the onset of these studies, there was no available information on human T lymphocyte responses to Old World hantaviruses. Virus-specific CD8+ and CD4+human T cell lines had been isolated from patients with acute HPS caused by Sin Nombre virus (SNV) infection. In that study, conducted in our laboratory, several human T cell epitopes on the nucleocapsid (N) protein and G2 envelope glycoprotein of SNV were identified and characterized. We decided to perform similar analyses on PBMC from donors who had been infected with HTNV and PUUV, in order to determine the specificity and diversity of the T cell response to Old World hantaviruses.
The initial study of three donors who had sub-clinical infections with HTNV demonstrated that virus-specific T cell responses could be detected in all the donors following in vitro stimulation of PBMC with inactivated virus. In two of the donors, the virus-specific cytolytic T cells (CTL) recognized the HTNV N protein, and in the third donor the virus-specific CTLs recognized the HTNV G1 glycoprotein. Isolation and characterization of virus-specific T cells from two donors resulted in the identification of two CD8+ T cell epitopes on the HTNV N protein, which were restricted by either HLA A1 or B51. These CTL lines included both HTNV-specific (HLA B51-restricted) and serotype-cross reactive (HLA A1 restricted) lines. In one subject, these virus-specific T cell responses were detectable in IFN-γ ELISPOT assays following peptide stimulation, and in bulk cultures after short-term stimulation with inactivated HTNV. These results indicated that the CD8+CTL responses of humans after sub-clinical infection with HTNV were readily detectable and were directed against a limited number of viral proteins and epitopes. In addition, sub-clinical infection resulted in the generation of both virus-specific and cross-reactive CTL responses.
We reasoned that hantavirus infections that lead to clinical illness may result in the generation of more robust and/or diverse virus-specific T cell responses than in sub-clinical infections. To address this question, we studied the memory CD8+ T cell responses in a group of healthy adults from Finland who had HFRS caused by PUUV infection between the years 1984 and 1995. We detected virus-specific CTL in the bulk cultures of seven of eleven immune individuals tested following stimulation with infectious virus. The PUUV proteins N, G1 and G2 were recognized by CTLs in six, five, and two donors respectively. Extensive cloning of T cells from two donors resulted in the isolation of sixty-three virus-specific CTL lines, the majority of which (61/63) were specific for the PUUV N protein. Six novel CD8+ CTL epitopes and one CD4+ CTL epitope were identified on the N protein, all of which clustered in the center of the protein between amino acids 173 and 251. The CTL lines specific for these epitopes were restricted by a variety of HLA alleles including A2, A28, B7 and B8, and were primarily serotype specific when tested against target cells expressing HTNV or SNV N protein. IFN-γ ELISPOT analysis using the defined epitopes to stimulated PBMC, revealed high frequencies of circulating N-specific CD8+ T cells in eight of thirteen individuals tested. Finally, T cell receptor (TCR) Vβ analysis of CTL clones specific for one epitope (N204-12) demonstrated that cells in this population expressed up to five different Vβ chains. These results demonstrated that the PUUV N protein may be the dominant target of the CTL response, that the N-specific CD8+ CTL responses are diverse, heterogeneous, and primarily serotype specific, and that virus-specific memory CD8+T cells can persist at high levels for up to 15 years after the primary infection.
In order to understand the pathology of HFRS and HPS, we must be able to assess the contribution of various factors that could potentially contribute to disease. The virus burden in the infected individual is likely to be an important factor in the severity of the resulting disease. Quantitative RT-PCR analysis of plasma samples from acute HPS patients demonstrated that a higher virus burden (as reflected by viral RNA copy number) is associated with more severe HPS. In order to perform similar analyses in patients with HFRS caused by PUUV, we established a quantitative RT-PCR assay for the detection of PUUV S segment RNA in patient plasma. The design and optimization of the PUUV-specific RT-PCR is described in this report. This assay will allow us to measure the virus burden in patients and compare these data with levels of T cell activation and with parameters of disease severity. In this way, we hope to gain an understanding of the kinetics and magnitude of both the virus burden and virus-specific T cell response during the acute illness.
This thesis provides the first description of human virus-specific T cell responses to HTNV and PUUV. These data shed light on the nature of the CD8+ T cell responses that are generated following natural infections with PUUV and sub-clinical infections with HTNV. The studies of memory CD8+ T cell responses to PUUV, and the development of a PUUV-specific quantitative RT-PCR assay, establish the framework for future studies of the immunopathology of acute HFRS. Quantitative analysis of both virus burden and T cell responses during acute illness will provide insight into their relative contributions to the pathology of disease.
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de, Jager Veronique Rejean. "Trends in the presenting clinical profile of patients with pulmonary tuberculosis in the Western Cape, 1991 - 2009." University of the Western Cape, 2017. http://hdl.handle.net/11394/6455.
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Magister Public Health - MPH (Public Health)Over the past two decades, despite a growing tuberculosis (TB) epidemic, the South African health system and National TB Programme (NTP) have taken significant steps to ensure improved clinical awareness, early diagnosis, prompt treatment initiation and follow-up of treatment outcomes in cases of TB. The effects of these programmatic measures over time on changes in the severity of disease and presenting clinical profile of patients with pulmonary TB have not been studied. Doing so may provide another window on the impact of TB control initiatives in South Africa.
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Gordon, Robert L. "A comparison of exhaled breath nitric oxide between old and young individuals." [Tampa, Fla.] : University of South Florida, 2004. http://purl.fcla.edu/fcla/etd/SFE0000346.
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Hui, Wai-san Teresa, and 許惠珊. "Clinical spectrum of aspergillus infections in Hong Kong." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206511.
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Aspergillus species are responsible for a variety of human diseases, ranging from allergic bronchopulmonary aspergillosis to invasive aspergillosis. Identification of Aspergillus species could facilitate the selection of antifungal regimens and epidemiological studies. Most of the clinical microbiology laboratories identify Aspergillus species by traditional phenotypic and/or antigen detection methods, which are laborious, time-consuming and inaccurate. In recent years, sequence analysis of β-tubulin and calmodulin genes becomes widely used for the identification of fungal species due to their relatively high resolving power, universality of usage, and high availability in the public databases. It can also be used for the taxonomic classification and the identification of rare and even novel fungal species. In this study, we aim to evaluate the effectiveness of analyzing the β-tubulin and calmodulin gene sequences for the identification of Aspergillus species and subsequently to determine the clinical spectrum of Aspergillus infections in Hong Kong during 2012-2014.
In this study, 48 Aspergillus strains isolated from patients over a 3-year period were characterised to the species level using sequencing of β-tubulin and calmodulin genes and the clinical spectrum of the 48 patients was described. Sequencing of β-tubulin and calmodulin genes showed that all 48 strains were known Aspergillus species. Ten different Aspergillus species were identified, including A. fumigatus (n=16), Aspergillus species of the A. flavus clade (n=7), A. awamori (n=7), A. terreus (n=6), A. tubingensis (n=4), A. sydowii (n=3), A. pseudocaelatus (n=2), A. uniguis (n=1), Aspergillus species of the A. tamarii clade (n=1), and A. austroafricanus (n=1). These Aspergillus species were shown to be associated with respiratory infections, infections of nail, ear canal infections, invasive infections, and eye infection. This study also described the first reported cases of ear infection associated with A. pseudocaelatus. To conclude, sequence analysis of β-tubulin and calmodulin genes enables accurate and rapid Aspergillus species differentiation.published_or_final_version
Microbiology
Master
Master of Medical Sciences
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Ho, Duy-Khiet [Verfasser], and Claus-Michael [Akademischer Betreuer] Lehr. "Novel anti-infective delivery systems for the treatment of pulmonary bacterial infections / Duy-Khiet Ho ; Betreuer: Claus-Michael Lehr." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2019. http://d-nb.info/1182989136/34.
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