Дисертації з теми "Lungs Immunology"
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Lemaitre, Philippe. "Early role of IL-17 and calcineurin inhibitor-mediated Th2- and Th17-polarization of chronic trachea allograft rejection pathways." Doctoral thesis, Universite Libre de Bruxelles, 2014. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209243.
Повний текст джерелаWe first demonstrated that interleukin-17 contributes to inflammatory lesions in the early phase post-transplantation. Interleukin-17 was found to be produced by &61543;&61540;+ T cells and CD4+ T cells infiltrating the graft and interleukin-17 neutralization significantly reduced the development of epithelial lesions together with inhibition of interleukin-6 and heat-shock-protein 70 gene transcription.
We then investigated the contribution of interleukin-17 to obliterative airway disease. Although interleukin-17 did not play a dominant role in absence of immunosuppression, it was found to contribute to airway pathology in animals receiving cyclosporin A. Under this treatment, we first observed dramatic changes in the composition of the lymphocyte populations infiltrating the graft: the numbers of CD8+ T cells producing interferon-&61543; and type 1 CD4+ T cells were dramatically decreased while the numbers of type 17, and also type 2 CD4+ T cells were unaffected. The pathological relevance of these findings was first demonstrated by the prolongation of graft survival afforded by the depletion of CD4+ T cells in cyclosporin A-treated animals. Furthermore, graft rejection was also delayed in mice genetically deficient in either interleukin-17 or interleukin-4, providing evidence that type 17 and type 2 CD4+ T cells actively contribute to graft rejection in cyclosporin A-treated recipients. On the other hand, parallel experiments in interferon-&61543;-deficient mice revealed that interferon-&
Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished
Vanderstocken, Gilles. "Caractérisation du rôle des nucléotides extracellulaires et du récepteur purinergique P2Y2 dans la physiopathologie des maladies pulmonaires inflammatoires." Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209591.
Повний текст джерелаhealth problem. As a consequence, investigating the immune mechanisms that contribute to
the pathogenesis of these diseases is essential to identify candidate targets for the
development of new therapeutic drugs. Furthermore, over the past 20 years, the growing awareness
that purinergic signalling events shape the immune and inflammatory responses to infection and
allergic reactions warranted the development of animal models to assess their importance in vivo in
acute lung injury and chronic airway diseases. The field of purinergic inflammation formulated the
unifying concept that ATP is released as a «danger signal» to induce inflammatory responses upon
binding purinergic receptors.
According to these elements, we began in 2007 to evaluate lung inflammation in mice deficient for
the P2Y2 purinergic receptor in TH2 and TH1 models. The most convincing evidence that the P2Y2
receptor is engaged during alarm situations comes from studies related to cystic fibrosis and asthma.
Indeed, chronic respiratory diseases are commonly associated with elevated airway ATP
concentrations, as reported in cystic fibrosis, but also in idiopathic pulmonary fibrosis and chronic
obstructive pulmonary disease (COPD) patients, and they are raised by allergens in asthmatic
patients.
First, we demonstrated a significant role of the P2Y2R in a TH2-ovalbumin(OVA)-induced asthma
model. We observed that eosinophil accumulation, a distinctive feature of lung allergic inflammation,
was defective in OVA-treated P2Y2-deficient mice compared with OVA-treated wild type animals.
Interestingly, the upregulation of VCAM-1 was lower on lung endothelial cells of OVA-treated P2Y2
knockout mice compared with OVA-treated wild type animals. Adhesion assays demonstrated that
the action of UTP on leukocyte adhesion through the regulation of endothelial VCAM-1 was
abolished in P2Y2-deficient lung endothelial cells. Additionally, the level of soluble VCAM-1, reported
as an inducer of eosinophil chemotaxis, was strongly reduced in the bronchoalveolar lavage fluid of
P2Y2-deficient mice.
Secondly, we studied the consequences of P2Y2R loss in lung inflammation initiated after pneumonia
virus of mice (PVM) infection in collaboration with the group of Pr. Daniel Desmecht (ULg). We
demonstrated here that P2Y2
-/-
mice display a severe increase in morbidity and mortality rate in
response to PVM. Lower survival of P2Y2
-/-
mice was not correlated with excessive inflammation
despite the higher level of neutrophil recruiters in their broncho-alveolar fluids. Interestingly, we
observed lower numbers of dendritic cells, CD4
+
T cells and CD8
+
T cells in P2Y2
-/-
mice compared to
P2Y2
+/+
infected lungs. Lower level of IL-12 and higher level of IL-6 in broncho-alveolar fluid support
an inhibition of Th1 response in P2Y2
-/-
mice. Quantification of DC recruiter expression revealed
comparable IP-10 and MIP-3&
Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished
Fallata, Ghaith Mohammed. "Association of gut luminal metabolites and allergic responses." Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright1515185113264117.
Повний текст джерелаTodd, Anthony. "The immunology of extrinsic allergic alveolitis : with reference to bird breeders' lung." Thesis, University of Newcastle Upon Tyne, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287418.
Повний текст джерелаRamis, Cabrer Daniel 1993. "From chronic obstructive pulmonary disease to lung cancer : an immunologic approach." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/667310.
Повний текст джерелаIt is well established that a subset of cancer patients debuts with immune infiltrates, which organize into aggregates in the tumor niche and its vicinity. These lymphoid structures develop in response to inflammatory stimuli through a tightly regulated process. Besides the prognostic value of TLSs, they also may represent a novel avenue for therapeutic strategies, but it is currently still in its early stages. In contrast with the immune activator role of TLSs, in certain cancers, its effect may point towards tumor progression as a consequence of highly tumor-mediated immunosuppressive conditions present in the tumor niche. Preliminary data provided by the current investigation suggests that a differential immune profile may be present between LC patients and LC patients underlying COPD. This fact could present a potential impact in the prognosis and therapy of these patients. Moreover, crucial markers targeting different signaling pathways involved with oxidative stress, apoptosis, and autophagy were found to be overexpressed in response to immunomodulators administration in the current thesis. These data puts into manifest the interest of additional immunity-related mechanisms that could be targeted in order to assist immunity against cancer.
Larsson, Emelie Olivia. "Immune to brain communication in allergic lung inflammation." Thesis, University of Southampton, 2013. https://eprints.soton.ac.uk/355709/.
Повний текст джерелаWhite, Anna-Marie. "The role of tumour necrosis factor α in lung inflammation". Thesis, University of Bath, 1996. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362198.
Повний текст джерелаSingh, Ravinder. "The role of Death Receptor 3 in allergic lung inflammation." Thesis, Cardiff University, 2014. http://orca.cf.ac.uk/56963/.
Повний текст джерелаArko-Mensah, John. "Mycobacterial infection: Immune evasion, host susceptibility and immunological markers of diagnostic importance." Doctoral thesis, Stockholm University, Wenner-Gren Institute for Experimental Biology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-8208.
Повний текст джерелаIIn the first study, we investigated the functional implications of prolonged TLR signalling on IFN-γ mediated killing of mycobacteria by murine macrophages in vitro. TLR2, but not TLR4 ligation interfered with IFN-γ mediated killing of mycobacteria in macrophages. In terms of mechanisms, neither TNF nor nitric oxide (NO) production was significantly affected, and the refractoriness induced could be reversed with increasing amounts of IFN-γ In the second study, we aimed to identify immunological markers of diagnostic importance in both the respiratory tract and serum during pulmonary mycobacterial infection in mice. We found that increased levels of immunological markers in the respiratory tract, but not serum, correlated better with active mycobacterial infection in the lungs, suggesting that the immune response in the respiratory tract is more reflective of the infection status and pathology than the systemic response. Finally, we investigated the level and nature of immune responses to pulmonary mycobacterial infection in BALB/c and C57BL/6 mice, two mouse strains known to exhibit different susceptibilities to infection with several intracellular pathogens, including mycobacteria. We showed that increased susceptibility of BALB/c mice to early mycobacterial infection was associated with reduced Th1 immune responses, and increased sTNFR secretion in the lung. Moreover, BALB/c mice recruited fewer monocytes/macrophages to the lung, and although IFN-γ stimulation of infected bone marrow derived macrophages in both mouse strains resulted in induction of antimycobacterial activity, BALB/c mice had a reduced capacity to kill ingested bacteria. The work presented in this thesis provide further insight into the mechanisms involved in the host-pathogen interaction; from persistence, to the immunological processes induced by the pathogen, to susceptibility of the host to infection.
Hosker, Harold Stephen Ronald. "Alveolar macrophage and blood monocyte function in small cell lung cancer." Thesis, University of Newcastle Upon Tyne, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241364.
Повний текст джерелаLambert, 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.
Повний текст джерелаDivangahi, Maziar. "Pseudomonas aeruginosa lung infection and respiratory muscle weakness : role of cytokines in diaphragm muscle dysfunction." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85903.
Повний текст джерелаBecause skeletal muscles can express a variety of immune modulating molecules such as cytokines, chemokines, adhesion molecules, and major histocompatibility molecules, the objective of the second study in this thesis was to study the possible role of pro-inflammatory cytokines in diaphragm muscle dysfunction in our animal model. Our results indicate for the first time that intra-diaphragmatic pro-inflammatory cytokine gene expression (TNF-alpha, IL-1alpha, IL-1beta, IL-6, and IL-18) is highly up-regulated in infected animals and the magnitude of such upregulation is dependent upon the dose of P. aeruginosa lung infection. Parallel to the absence of muscle contractile dysfunction in hindlimb muscle under the same conditions, P. aeruginosa infection did not alter the levels of pro-inflammatory gene expression within the hindlimb muscle. To further address the involvement of muscle-derived pro-inflammatory cytokines in diaphragmatic contractile dysfunction, we have employed recombinant adenovirus (Ad) as a vehicle for systemic delivery of the anti-inflammatory cytokine IL-10, in order to shift the balance between pro- and anti-inflammatory cytokines within the diaphragm toward a more anti-inflammatory profile. We report here that systemic delivery of Ad-IL-10 suppresses pro-inflammatory gene expression and improves force generating capacity of the diaphragm in P. aeruginosa infected animals. This finding emphasizes the role of anti-inflammatory cytokines as beneficial immune modulators in respiratory muscle failure caused by pro-inflammatory cytokines.
P. aeruginosa lung infection is a major cause of morbidity and mortality among cystic fibrosis (CF) patients and many patients with CF have weak peripheral and respiratory muscles. Although the role of pro-inflammatory cytokines has been extensively studied within the lungs of CF patients, the involvement of these cytokines in skeletal muscle dysfunction in animal models of CF or in human CF patients has not been studied. Therefore, in the third study of this thesis we have used mice sharing the same genetic defect as CF patients (Cftr knockout mice), in combination with our model of P. aeruginosa lung infection, to address several fundamental questions related to muscle function in CF. Our first objective in this portion of the thesis was to determine if diaphragmatic skeletal muscle cells express the CFTR mRNA. Our second objective was to ascertain whether intrinsic differences between CF and wild-type muscle cells could be detected in vitro, which might differentially affect the regulation of pro-inflammatory mediators in the setting of infection/inflammation. Our third objective was to evaluate possible differences in the ability of respiratory muscles to generate force prior to and after P. aeruginosa lung infection in Cftr knockout mice, as compared to their wild-type littermates. Finally, we aimed to determine if the absence of CFTR expression would predispose to muscle dysfunction triggered by up-regulation of intra-diaphragmatic pro-inflammatory gene expression. Our major results indicate that: First, in vitro stimulation with pro-inflammatory cytokines (TNF-alpha, IL-1alpha, and IFN-gamma) and LPS (extracted from Pseudomonas aeruginosa) triggered increased expression of pro-inflammatory mediators (iNOS, RANTES, MIP-1alpha, MIP-1beta, MIP-2 and KC) in both Cftr -/- and wild-type diaphragmatic myotubes, but the magnitude of cytokine/chemokine upregulation was significantly greater in CF than in wild-type diaphragm muscle cells. Sec
In the final study of this thesis, we sought to test the hypothesis that increased diaphragm muscle activation would lead to increased production of intra-diaphragmatic cytokine expression, since this could possibly explain the greater susceptibility of the diaphragm to express pro-inflammatory cytokines in response to pulmonary P. aeruginosa infection as compared with the hindlimb muscle. To test this hypothesis, we subjected rats to inspiratory resistive loading (IRL), corresponding to 45-50% of the maximum inspiratory pressure, and described that mRNA levels of IL-1beta, IL-6, and to a lesser extent, IL-4, IL-10, TNF-alpha, and IFN-gamma were all significantly increased in a time-dependent fashion in the diaphragm but not hindlimb muscle (gastrocnemius) of loaded animals. In addition, elevated protein levels of IL-1beta and IL-6 in response to loading were confirmed with immunoblotting and immunostaining. We also detected significant IL-6 protein to be localized inside diaphragmatic muscle fibers of loaded animals. We conclude that increased diaphragm muscle activity during resistive loading induces upregulation of pro-inflammatory cytokine gene expression in the diaphragm, which could also provide an explanation for the greater cytokine expression observed in the diaphragms of animals with P. aeruginosa lung infection.
Bull, Naomi. "The role of lung tissue-resident memory T cells in protection against tuberculosis." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:45ee10ce-0ca3-4459-9da8-5cf9078f2cbb.
Повний текст джерелаBasich, Dinko. "The role of IL-4Rá in Nippostrongylus brasiliensis-induced chronic lung pathology." Master's thesis, University of Cape Town, 2010. http://hdl.handle.net/11427/13437.
Повний текст джерелаInfection by the parasitic nematode Nippostrongylus brasiliensis involves migration through the lungs, causing significant damage and generating chronic lung pathology. The resolution of N. brasiliensis infection and also the induction of pulmonary pathology, including goblet cell hyperplasia and acute airway inflammation, depend on IL-4Rá signalling. A key feature of IL-4Rá signalling is the induction of a strong TH2 response which induces the development of alternatively activated macrophages (AAMs). AAMs are associated with tissue remodelling and the control of exacerbated inflammation. In order to investigate potential roles for IL-4Rá in N. brasiliensis' induced lung pathology, we infected mice deficient for IL-4Rá on macrophages and neutrophils (LysMCreIL-4Rá-/lox), IL-4Rá -/- and control mice (IL-4Rá-/lox) with N. brasiliensis and examined lung pathology at days 5, 42 and 180 post infection (p.i.).All three mice strains showed similar emphysemic-like pathology (alveolar dilatation) and airway hyperresponsiveness (AHR) which was well developed by day 42 p.i. and remained chronic. However, LysMCreIL-4Rá-/lox mice consistently demonstrated earlier and increased pulmonary inflammation when compared to IL-4Rá-/lox control mice and IL-4Rá-/- mice. Immunological studies at day 5 p.i. revealed that there were increased CD4+ and CD8+ T-cell numbers and increased CD4+ IL-4 and IL-13 production in the lungs of LysMCreIL-4Rá-/lox mice when compared to control and IL- 4Rá-/- mice. LysMCreIL-4Rá-/lox mice also showed decreased pulmonary arginase activity, indicative of a reduction of AAMs. RNA transcript analysis of isolated alveolar macrophages showed a strong association with promoting inflammation in LysMCreIL-4Rá-/lox mice. Together these data demonstrate that IL-4Rá-responsive macrophages control pulmonary inflammation and play an important protective role in the lung following N. brasiliensis infection.
McCaughey, Laura C. "The development of pyocins as novel antimicrobials for the treatment of Pseudomonas aeruginosa lung infection." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/6497/.
Повний текст джерелаHuang, Jing-Qi. "The immunoreactive expression of neuroendocrine cells or neuroendocrine bodies in human chronic lung disease /." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61879.
Повний текст джерелаMendoza, Valderrey Alberto. "Cross-platform biomarker signature of long-term survival with normal allograft function after lung transplantation." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/670678.
Повний текст джерелаEl trasplante pulmonar (TP) es el tratamiento de elección en enfermedades respiratorias terminales. La supervivencia a corto plazo tras el mismo ha ido aumentando progresivamente debido a las mejoras en las técnicas quirúrgicas, la preservación de órganos, las terapias inmunosupresoras y el manejo perioperatorio. Sin embargo, el desarrollo de la disfunción crónica del injerto pulmonar (DCIP) representa el principal factor limitante para alcanzar la supervivencia a largo plazo tras el TP, siendo la tasa de supervivencia a diez años aproximadamente de un 34.3%. El tratamiento inmunosupresor de por vida en los pacientes trasplantados de órgano sólido conlleva una serie de complicaciones (nefrotoxicidad, infecciones, aparición de cáncer y/o desórdenes metabólicos) que influyen negativamente en su supervivencia a largo plazo. Uno de los principales objetivos en el trasplante de órganos es conseguir la falta de respuesta inmunológica del receptor frente al injerto en ausencia de terapias inmunosupresoras sostenidas. En la mayoría de los casos, la retirada de la inmunosupresión conlleva el rechazo del injerto. Sin embargo, se ha observado que un pequeño grupo de pacientes mantiene una buena función del injerto a largo plazo a pesar de la interrupción del tratamiento (tolerancia operacional). Este estado es infrecuente y únicamente se han observado casos en pacientes trasplantados renales y de hígado. En otros trasplantes de órgano sólido (pulmón, corazón o intestino) solo se han reportado casos anecdóticos de este fenómeno. Dada la falta de pacientes trasplantados pulmonares con tolerancia operacional, los supervivientes a largo plazo (SLP) con una buena función del injerto tras el TP son el grupo que más se asemeja a los tolerantes operacionales tras el trasplante de riñón o de hígado. La identificación de biomarcadores de tolerancia operacional permitiría la precisa selección de aquellos pacientes candidatos a la minimización y potencial retirada del tratamiento inmunosupresor. Además, estos potenciales biomarcadores podrían proporcionar conocimiento acerca de los mecanismos biológicos que subyacen a la tolerancia y podrían usarse en el desarrollo de nuevas terapias tolerogénicas. Se ha observado que las firmas de tolerancia en riñón e hígado difieren, sugiriendo que los mecanismos responsables de la tolerancia operacional son órgano-específicos y que los potenciales biomarcadores de tolerancia no pueden extrapolarse al caso del pulmón. Dado los escasos estudios publicados sobre la supervivencia a largo plazo con buena función del injerto tras el TP, el objetivo de esta tesis es analizar el mayor número de parámetros clínicos e inmunológicos a través de diferentes plataformas para la identificación de potenciales biomarcadores, y así, proporcionar nuevo conocimiento sobre los mecanismos biológicos responsables de la supervivencia a largo plazo con buena función del injerto en comparación con pacientes con DCIP. El microbioma de las vías respiratorias altas y el completo perfil transcriptómico e inmunofenotipado en sangre periférica fue analizado para evaluar las características de los pacientes SLP. Los resultados derivados de los análisis bioinformáticos correspondientes a la expresión génica y de microRNAs proporcionaron nuevos datos referentes a los mecanismos implicados en la supervivencia a largo plazo. Además, se consiguió clasificar a los pacientes trasplantados pulmonares con alta precisión empleándose para ello perfiles de expresión génica y de expresión combinada de varios biomarcadores. En conclusión, los estudios incluidos en la presente tesis han demostrado la utilidad del uso del perfil transcriptómico y de las muestras de sangre periférica para discriminar a los pacientes SLP y con DCIP y para identificar potenciales mecanismos responsables de la aceptación del injerto a largo plazo, proporcionando nuevas perspectivas para futuras investigaciones en la inmunología del TP.
Lung transplantation (LT) is an established treatment for end-stage respiratory diseases. Short-term survival has progressively improved due to advancements in surgical techniques, donor preservation, immunosuppressive agents and perioperative management. However, the development of chronic lung allograft dysfunction (CLAD) is the main limiting factor of long-term success after LT, with an approximate ten-year survival rate of 34.3%. The lifelong immunosuppression of solid organ transplant patients leads to severe complications, such as nephrotoxicity, infectious diseases, malignancies, and metabolic disorders, which poorly affect their long-term survival. For this reason, one of the main goals in organ transplantation is achieving an alloantigen-specific unresponsiveness state in the sustained absence of toxic immunosuppressive therapies. In most cases, immunosuppression withdrawal leads to transplant rejection. However, a small group of transplant patients maintains long-term stable graft function despite interrupted treatment (operational tolerance state). This phenomenon is infrequent and varies according to the type of allograft; excluding kidney and liver transplant fields, there are only anecdotal cases in lung, heart and intestine transplantation. Due to the lack of operationally tolerant lung transplant recipients, long-term survivors with normal allograft function (LTS) after LT are the closest group to “operational tolerance” of kidney or liver transplant patients. Identifying biomarkers of operational tolerance would serve to accurately identify candidate patients for minimization and potential withdrawal of immunosuppression. Furthermore, these potential tolerance biomarkers could provide knowledge of the underlying biological mechanism of tolerance for new tolerogenic therapies. It has been observed that tolerance fingerprints from kidney and liver transplant recipients differ, suggesting that the underlying mechanisms of operational tolerance, not fully elucidated, are organ-specific and consequently, potential renal and liver tolerance biomarkers cannot be extrapolated to lung. Since no extensive studies examining this LT state have been published, the main objective of this thesis was to screen the greatest number of clinical and immunological parameters to identify potential biomarkers across different platforms in order to provide a better understanding of the biological mechanisms underlying LTS with normal allograft function after LT in comparison with CLAD patients. The microbiome of the upper respiratory tract and the full transcriptomic expression profile and extensive cell immunophenotyping of peripheral blood samples were studied to assess the particular characteristics of LTS patients. The results derived from bioinformatics analyses of gene and miRNA expression provided a better understanding of the mechanisms involved in long-term survival. Moreover, they proved to be highly accurate in the classification of LT patients by employing gene and multi-biomarker expression profiling using different transcriptional platforms, including microarrays and RT-qPCR arrays. The findings obtained demonstrated the usefulness of global transcriptome profile and peripheral blood samples to differentiate between LTS and CLAD patients and to identify some of the potential mechanisms responsible for graft acceptance. Overall, the studies included in this thesis shed light on the biology underlying graft acceptance after LT, suggesting a complex interaction of several immunological mechanisms and opening up new perspectives for future research in LT immunology.
Qaseem, Asif Shehzad. "Modulation of immune cell functions by human lung surfactant protein SP-D in allergic asthma." Thesis, Brunel University, 2016. http://bura.brunel.ac.uk/handle/2438/13893.
Повний текст джерелаFoley, Corinne L. "Immune and pulmonary dysfunction associated with human STAT5B deficiency." University of Cincinnati / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1623165242584526.
Повний текст джерелаIsaacs, Travis. "LPS induced chorioamnionitis promotes IL-1 and TNF dependent recruitment of MAIT cells in fetal lung." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1592171436262216.
Повний текст джерелаBetts, Catherine Jean. "RT-PCR analysis of cytokine expression in murine lymph node and lung tissue following exposure to the irradiated Schistosoma mansoni vaccine." Thesis, University of York, 1996. http://etheses.whiterose.ac.uk/10876/.
Повний текст джерелаTravaillé-Aubert, Christelle. "Paludisme en zone d'hyperendémie : apport de la réponse cytokinique et transcriptomique." Thesis, Aix-Marseille, 2013. http://www.theses.fr/2013AIXM5022/document.
Повний текст джерелаAmong complications of the malaria access, mostly due to P. falciparum, the pulmonary injuries are often underestimated. Despite numerous studies trying to better understand the inflammatory mechanisms involved in disease worsening, they are still poorly understood. In view to study the host-parasite interactions and identify biomarkers according to severity of malaria, a prospective longitudinal cohort study was carried out in Monkole Hospital (Kinshasa) through a combined immunological and transcriptomic approach, with a follow up on 30 days. Initially, the study concerned the pulmonary injuries, but was focused on the the severity of malaria because of a weak patients number with lung damages.The immunological approach highlighted a moderate Th1 pro-inflammatory response at admission. The transcriptomic approach allowed to connect it with a moderate activation of monocytes/macrophages, mediated by IL-12 signaling pathway, higher in severe malaria. Malaria infection, particularly severe malaria, appears to be strongly dependent on Th17 response, especially to neutrophil activity. The establishment of a Th2 response is also observed in malaria patients. On day 7, Th2 response is predominant, associated with significant hematopoietic activity. On day 30, patients are cured and present a similar profile to healthy controls.These results have to be confirmed with an increased cohort
Sundaram, Kruthika. "Expression And Function Of Human IkappaBzeta In Lung Inflammation." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1436224271.
Повний текст джерелаShestowsky, William S. "Production and characterization of a monoclonal antibody to a highly metastatic and organ-selective variant of the Lewis lung carcinoma." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61747.
Повний текст джерелаChen, Gang. "Critical roles of Foxa2 and Spdef in regulating innate immunity and goblet cell differentiation in the lung." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1276537438.
Повний текст джерелаTweedle, Jamie L. "TNF Antagonism Stifles Host Response to Pulmonary Pathogen through Gut/lung Immunoregulatory Axis." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1535457070656335.
Повний текст джерелаHernandez, Yeritza I. "Retinoic Acid synthesis by lung antigen presenting cells and induction of its synthesis by Mycobacterium tuberculosis." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1387807076.
Повний текст джерелаSlater, Tessa. "Bat lung epithelial cells show variable species-specific susceptibility to human and avian influenza viruses." Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/49403/.
Повний текст джерелаWindsor, Alastair Colin James. "An investigation of the role of tumour necrosis factor alpha in gram negative sepsis : defining a link between sepsis and neutrophil mediated acute lung injury." Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306899.
Повний текст джерелаKoloze, Mary T. "The Role of Matrix Metalloproteinases (MMPs) and their Proteolytic Degradation of Chemokines in the Lung." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1269959847.
Повний текст джерелаHeil, Luke. "THE ROLE OF CD8 T CELL IMMUNODOMINANCE AND REGULATORY T CELLS IN NEONATAL IMMUNITY TO INFLUENZA VIRUS." UKnowledge, 2019. https://uknowledge.uky.edu/microbio_etds/22.
Повний текст джерелаAl-Kerithy, Mohammed. "Role of IL-17 and IL-11 in immunopathology of chronic rejection post-lung transplantation." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=81260.
Повний текст джерелаThe objectives of the study were to investigate the expression of IL-11 and IL-17 (mRNA and protein) in endobronchial biopsies from lung transplant patients and to define the correlation between the expression of IL-11 and IL-17 and the development of chronic rejection.
Meikle, Claire K. "Platelet-Leukocyte Aggregation in Lung Cancer Patients." University of Toledo Health Science Campus / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=mco1555937904448281.
Повний текст джерелаWhitacre, 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.
Повний текст джерелаDeGrace, Marciela. "RNAi Screens in Primary Human Lung Cells Reveal Hermansky-Pudlak Syndrome Proteins as Influenza Suppressors." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10152.
Повний текст джерелаSaunders, Vanessa C. "Mechanisms of Particulate Matter-Induced Experimental Asthma." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1267738359.
Повний текст джерелаFrançois, Antoine. "Rôle du "B-cell activating factor" (BAFF) et des lymphocites B dans la fibrose pulmonaire et cutanée dans la sclérodermie systémique." Thesis, Strasbourg, 2013. http://www.theses.fr/2013STRAJ056/document.
Повний текст джерелаSystemic sclerosis (SSc) is a rare autoimmune disease characterized by skin fibrosis and occasionally pulmonary fibrosis. We first assessed the role of BAFF, a cytokine involved in B cell maturation, in bleomycin-induced pulmonary fibrosis in mice. We showed that BAFF was increased in response to bleomycin and that BAFF-/- mice or BAFF-R-Igtreated mice are protected from pulmonary fibrosis. Then, we assessed whether B cells and BAFF could regulate collagen production by skin fibroblasts isolated from SSc patients. We demonstrated that B cells increase collagen production and cytokines involved in skin fibrosis. The addition of BAFF increases the effect of B cells on fibroblasts. Lastly, we studied the regulation of BAFF expression by microRNAs. Our results show that miR-30a*, d* and e* directly target the BAFF mRNA
Charrier, Mélinda. "Caractérisation phénotypique et fonctionnelle de sous-populations Natural Killer (NK) chez des patients atteints d’un cancer bronchique non à petites cellules et impact d’une vaccination avec des exosomes de cellules dendritiques (Dex) autologues." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS438.
Повний текст джерелаRecently, immunotherapy has emerged as a new strategy in Non-Small Cell Lung Cancer (NSCLC) patients, confirming the key role of the immune system in this disease. Despite these new treatments (targeted therapies, immunotherapy), response rates remain low with a modest impact on overall survival. Biomarkers are needed to define the target population of these treatments. One of the options explored is the immune status; indeed the immune status of cancer patients has a prognosis impact and may influence the response to standard treatments such as chemotherapy, targeted therapies and even immunotherapy. Among the immune cells, Natural Killer cells (NK) have an effector role in NSCLC. It is now established that NK cells can promote a functional and efficient adaptive immunity. Therefore, an impaired NK functions could be a mechanism associated with the escape from adaptive immunity of the tumor. In our first study, we demonstrated that exosomes from dendritic cells stimulated NK cells through NKp30, this activity is being associated with improved survival in advanced NSCLC. Our second project has revealed, for the first time, a independent prognostic role of NCR3 transcript (NKp30 gene) for naïve advanced NSCLC. Activation of NK cells via NKp30 could be an effective strategy for immunomodulation in advanced NSCLC patients. These studies confirm a major role of NK cells in advanced NSCLC
Pandey, Sumali. "Lung mucosal response to repeated inhalational insults with immunomodulatory agents in a murine model of fungal asthma| Airway epithelium takes the center stage." Thesis, North Dakota State University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3603972.
Повний текст джерелаAsthma is a debilitating disease of the lungs affecting 235 million people worldwide. Fungus-associated asthma leads to a particularly severe type of disease, and exposure to environmental fungi and their products is unavoidable due to the ubiquitous nature of fungal species. Besides being allergenic, fungi are opportunistic pathogens, and anti-fungal and/or allergic pathways may be modified through repeated inhalation of immunomodulatory agents, affecting the outcome of fungus-induced asthma.
Our aim in this project was to investigate the extent to which repeated inhalation of immunomodulatory agents influence the lung mucosal responses in a naïve murine host or in one that had been sensitized to fungal proteins (allergic). The immunomodulatory substances chosen hold relevance to human inhalational exposure, and included live or irradiation-killed Aspergillus fumigatus (a fungi) spores, deoxyxnivalenol (a mycotoxin), and fluticasone propionate (an inhalationally administered corticosteroid, commonly prescribed for allergic asthma). In a naïve host, inhalation of live A. fumigatus spores showed pathological features of fungal asthma. However, in an allergen-sensitized lung, both dead and live A. fumigatus spores established fungal airway disease, albeit to different extents. Next, we tested the effect of deoxynivalenol in an allergic host and found that its repeated inhalation did not affect pulmonary disease pathology, but did lead to a dose- and time- dependent increase in mucosal and systemic total IgA. Finally, we tested the effect of fluticasone propionate, and found that it did not influence the development of fungal airway disease, but did induce dynamic changes in lung physiology and antibody titers.
Besides mimicking human inhalational exposures, inhalation ensures direct interaction of the inhaled substances with airway epithelium, which plays an important role in defense against inhaled substances and in asthma pathophysiology. By analyzing various mechanisms involved in murine lung-mucosal response to the inhaled substances, a critical involvement of airway epithelium as an orchestrator of immune responses is highlighted, and this would inform mechanism-based future studies. In conclusion, this project is likely to aid in establishing evidence based standards for fungus-related exposures and in making informed therapeutic decisions for fungus-associated diseases.
Campanholle, Gabriela. "O papel do receptor B1 da bradicinina em modelos experimentais de lesão pulmonar aguda direta e indireta." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-15122010-112737/.
Повний текст джерелаThe acute lung injury (ALI) is characterized by lung inflammation and can be induced directly by lipopolysaccharides inhalation, or indirectly, by systemic inflammatory mediators released from distant organs after and ischemia and reperfusion injury (IRI). Bradykinin, an inflammatory mediator, can act in two different receptors; one is constitutive (B2R), whereas the other is induced by inflammatory cytokines (B1R). We aimed to study the role of B1R in models of direct and indirect ALI. Direct ALI was induced by LPS instillation in C57bl/6 mice, while indirect ALI was induced by 45 minutes of renal IRI. In both injuries, 24 hours after insult, animals presented an increase in cellular infiltration, vascular permeability, hyperreactivity to methacholine, and an up-regulation of pro-inflammatory cytokines in lungs. We blocked the B1R using antagonist and observed that the lung injury was attenuated in both injury models. Thus, we suggest that B1R has an important role in the development of both, direct ALI, induced by LPS, and indirect ALI induced by renal IRI.
Cox, Jr Ruan Rollin. "Aspirin Triggered Resolution Phase Interaction Product D1: A Novel Treatment for Hyperoxic Acute Lung Injury." Scholar Commons, 2015. http://scholarcommons.usf.edu/etd/5931.
Повний текст джерелаBarlow, Peter George. "The effects of air pollution particles on clearance mechanisms within the lung." Thesis, Edinburgh Napier University, 2004. http://researchrepository.napier.ac.uk/Output/1052591.
Повний текст джерелаEppert, Bryan L. "Autoimmune Mechanisms in Cigarette Smoke-Induced Inflammation and Pathology." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1382950967.
Повний текст джерелаThiel, Bonnie Arlene. "Bioinformatics approaches to studying immune processes associated with immunity to Mycobacterium tuberculosis infection in the lung and blood." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1627247387242562.
Повний текст джерелаRonan, Edward. "Understanding vaccine induced protective immunity to Mycobacterium tuberculosis." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:c0d7b20f-e144-42f8-aa52-301d0938b0b3.
Повний текст джерелаVijay, Rahul. "Prostaglandin regulation of immune responses against coronavirus infections." Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/3209.
Повний текст джерелаScordo, Julia Marianna. "Impact of the Human Lung Mucosa on Mycobacterium tuberculosis Infection of Alveolar Epithelial Cells." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1542718137103233.
Повний текст джерелаHemann, 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.
Повний текст джерелаSchmidt, Megan Elizabeth. "Assessing T cell responses in respiratory syncytial virus infection and vaccination." Diss., University of Iowa, 2019. https://ir.uiowa.edu/etd/6850.
Повний текст джерелаBrodeur, Tia Bumpus. "Regulation of Type II Responses in Lung Fibrosis and Systemic Autoimmunity: A Dissertation." eScholarship@UMMS, 2014. https://escholarship.umassmed.edu/gsbs_diss/736.
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