Dissertations / Theses on the topic 'Neutrophils'
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Gillis, Caitlin. "Neutrophils in IgG- and endotoxin-induced systemic inflammation : protective or pathological agents ?" Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066279/document.
Full textNeutrophils are agents of protective and pathological inflammation. This thesis work aimed to determine the role of neutrophils during severe, potentially fatal models of systemic inflammation induced by lipopolysaccharide (LPS, endotoxemia) or by IgG immune complexes (anaphylaxis). Anaphylaxis is a severe allergic reaction that may proceed via IgE- or IgG-dependant pathways. Endotoxemia is a model relevant to inflammation during critical illness. To study neutrophils in vivo, we employed a new mouse model of inducible neutropenia. We found, surprisingly, that neutrophils and neutrophil-derived MPO protect against the severity of endotoxic shock, independently of the microbiological environment, suggesting that neutrophils limit inflammation during endotoxemia. Conversely, neutrophils can contribute to IgG-induced anaphylaxis in mice. As mice and human IgG receptors (FcγR) are very different, we developed a novel mouse strain in which targeted insertion of human FcγR into the murine loci recapitulated hFcγR expression. Herein, using these mice, this work demonstrates that anaphylaxis induced by hIgG proceeds within a native context of activating and inhibitory hFcγRs, and that neutrophil activation via FcγRIIA is a dominant pathological pathway, involving the mediators PAF and histamine. Finally, we describe ongoing development of a mouse model of anaphylaxis in response to Rocuronium, a curare-based neuromuscular blocking agent (NMBA). In addition, as part of a collaborative clinical study we analysed blood samples from patients suspected of NMBA-induced anaphylaxis, finding evidence for the activation of a neutrophil- and IgG-dependent axis during human anaphylaxis
Garcia, Geoffrey. "Les NETs (Neutrophils Extracellular Traps) et les DNases au cours de la COVID-19." Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0175.
Full textNeutrophil Extracellular Traps and DNases involvement during During infection, neutrophils release Neutrophil Extracellular Traps (NETs) to capture,prevent the dissemination of, and kill pathogens. NETs contribute to immunothrombosis byinteracting with platelets and immune cells, thus activating coagulation. However, excessiveproduction of NETs can cause thromboinflammation, leading to cellular and tissue damage. NETsare implicated in the pathophysiology of both arterial and venous thrombosis and in severe formsof COVID-19. They are physiologically degraded by DNases and macrophages. Currently, DNasetechniques are not standardized, and the mechanisms underlying the exacerbation of NETosis inCOVID-19 are not well understood. We first aimed to develop a functional assay to evaluate theability of DNases in human samples to degrade DNA or NETs. We established a robust,repeatable, and reproducible method that can be applied to both serum and plasma.Subsequently, we assessed the balance between NET markers and DNase activity according toCOVID-19 severity, and studied the mechanisms responsible for the NETs/DNases imbalance. Weconfirmed that NET markers increase with disease severity and demonstrated a decrease inDNase activity in hospitalized patients, resulting in an imbalance between NET markers andDNase activity in this group. The most severe patients exhibited decreased levels of DNase 1,with some harboring polymorphisms in the DNase 1 gene correlating with low protein levels.Additionally, we observed that critically ill patients had lower levels of plasmacytoid dendriticcells compared to those with severe disease. Reanalysis of public single cell RNA sequencing datashowed that plasmacytoid dendritic cells express less DNase 1L3 RNA as the disease severityincreases. This study demonstrates that COVID-19 severity is associated with an imbalance inNETs and DNases. Identifying this DNase deficit as an aggravating factor in patients could lead tonew therapeutic strategies, such as DNase administration, to prevent clinical deterioration
Mawhin, Marie-Anne. "Role of neutrophils and leukotrienes in atherosclerotic plaque destabilisation : implication of endotoxemia." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ034/document.
Full textAtherosclerotic plaque destabilisation remains an important issue, in spite of the recent advances in its comprehension. Neutrophils are powerful innate immune actors capable of altering plaques. In this context, the leukotriene B4, one of the main chemoattractants of neutrophils, has been proposed as a potential contributor to plaque destabilisation. A particular context in which these two actors are closely linked is endotoxemia, itself associated with plaque destabilisation This work was aimed at determining whether leukotriene B4 plays a role in the chemoattraction of neutrophils in plaques during endotoxemia and at assessing whether neutrophils can tip the balance which maintains plaques stable. We have herein evidenced that the recruitment of neutrophils mediated by leukotriene B4 has a deleterious impact upon plaque stability during endotoxemia by promoting apoptosis and degrading matrix fibres. In conclusion, this study paves the way to novel therapeutic approaches aimed at targeting the axis leukotriene-neutrophil in atherosclerotic disease
Yao, Yi. "Sequential Priming of Neutrophils." University of Toledo Health Science Campus / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=mco1389612809.
Full textManriquez, Rojas Valeria. "Role of the innate immune response in vascular damage caused by Neisseria meningitidis infection Vascular colonization by Neisseria meningitidis triggers a delayed and inefficient neutrophil response Intermittent pili-mediated forces fluidize Neisseria meningitidis aggregates promoting vascular colonization Adhesion to nanofibers drives cell membrane remodeling through 1D wetting." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB076.
Full textNeisseria meningitidis is a gram-negative diplococcus responsible for meningitis and septic shock. While meningitidis is the most frequent form of infection, fulminant septicemia is responsible for 90% of the mortality imputable to N. meningitidis. Meningococcal sepsis is characterized by a purpuric rash due to vascular damages. Observations at the histological level reveal meningococci associated to endothelial cells, thrombosis, perivascular hemorrhage and inflammatory cells infiltrates. The mechanisms leading to this vascular damage and the reasons for which the innate immune system is unable to control the infection before reaching this pathological stage are unknown. In this doctoral work, we address these questions using a humanized skin xenograft mouse model of Neisseria meningitidis infection. We report that bacterial proliferation inside capillaries is rapid leading to vessel occlusion in less than 3 hours post-infection. In this context, perivascular macrophages play a role of sentinels as they efficiently phagocytose adhering intraluminal bacteria at early stages of infection and are essential to recruit neutrophils to the site of infection. Intravital imaging and neutrophils depletion experiments indicate that neutrophils play an important role in killing adherent bacterial through a reverse migration process and as a consequence decrease the vascular damages induced by the bacteria. Interestingly, detailed analysis of the kinetics of neutrophil recruitment show that while neutrophil numbers reach a peak between 16h and 24h post-infection in mice challenged by the intravascular route as during the natural infection, this takes only 3h when bacteria are injected intra-dermally. These results show that intraluminal detection of bacteria by perivascular macrophages eventually leads to neutrophil recruitment and vascular damage control but this perivascular macrophage-dependent response is initiated too late to be fully efficient
Fischer, Steven Harold. "Interactions of Neisseria gonorrhoeae with human neutrophils: Gonococcal outer membrane protein II modulates neutrophil responses." Diss., The University of Arizona, 1988. http://hdl.handle.net/10150/184364.
Full textGRIMOLIZZI, FRANCO. "Neutrophils alter placental glucose metabolism in gestational diabetes mellitus via neutrophil elastase mediated IRS1 degradation." Doctoral thesis, Università Politecnica delle Marche, 2017. http://hdl.handle.net/11566/245194.
Full textHuman pregnancy is associated with a mild pro-inflammatory state characterized by activation of circulatory neutrophils (PMNs). Skewing of PMNs responses toward to neutrophil extracellular traps generation (NETs) is reflected in an increased of circulating nucleosomes and myeloperoxidase with advancing gestational age. Our data indicated that this pro-NETotic profile is enhanced in women with gestational diabetes mellitus (GDM). Maternal hyperglycemia and increased levels of TNF-a are a hallmark of GDM and we show a synergistic effect of both factors on the priming and release of NETs. Moreover, we hypothesized that systemic activation was associated with activated PMN in placenta. Indeed, we observed a massive infiltration of pro-NETotic PMNs and neutrophil elastase (NE) accumulation along chorionic villi of GDM placentas. To further explore whether hyperglycemia predisposes to exaggerated inflammatory response in placenta we incubated trophoblast BeWo cells in high glucose conditions and we next tested the TNF-a production capacity. Interestingly, TNF-a level was incresed and exert a pro-NETotic effect on PMN with consequent NE release. Recent studies in cancer tissues and diabetes models have described that released NE induce profound changes in the surrounding cells, altering the signal transducing cascade and promoting insulin resistance via degradation of insulin receptor substrate 1 (IRS1). Our in-vitro data indicate that addition of NE to trophoblast cell line BeWo causes degradation of IRS1 with consequent glucose uptake impairment. IRS1 is reduced in GDM placentas when compared to control placentas, suggesting that the presence of NE might be the causal factor. Taken together, our data showed that GDM is characterized by excessive NET formation and by a massive influx of pro-NETotic PMN into placentas. These findings underline the competence of NETs as a highly relevant diagnostic biomarker for GDM and NE as a new potential therapeutic target.
Darbousset, Roxane. "Roles of polymorphonuclear neutrophils in thrombosis." Thesis, Aix-Marseille, 2013. http://www.theses.fr/2013AIXM5071.
Full textHemostasis is a physiological process to preserve the integrity of the vascular system and to prevent blood loss in response to injury. In pathological conditions, such as cancers, infections or cardiovascular diseases, the blood coagulation cascade can be activated, leading to the formation of a platelet thrombus.Using a laser-injury model coupled with a high-definition, high-speed camera, we explored the cellular and molecular mechanisms involved in thrombus formation in physiological and in pathological conditions associated with the development of a cancer. The first part of this work describes the role of polymorphonuclear neutrophils (PMNs) in thrombus formation. We show that PMNs are the first cells to accumulate at the site of injury and represent the main source of blood-borne tissue factor (TF), leading to the generation of fibrin and thrombus formation. We also show that once present at the site of injury, PMNs recruit Endothelial Progenitor Cells (endothelial colony-forming cells, ECFCs), which play a key role in vascular repair. The second part of this work we determined, in dedicated mouse models, the involvement of TF and platelet activation in thrombosis associated with cancer. Together, our findings provide new perspectives in the understanding of the pathophysiological role of polymorphonuclear neutrophils, Endothelial Progenitor Cells and platelets
Haynes, Andrew Paul. "Metabolic abnormalities in uraemic neutrophils." Thesis, University of Nottingham, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305133.
Full textCross, Andrew. "Molecular properties of inflammatory neutrophils." Thesis, University of Liverpool, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250467.
Full textMacLeod, Ronald. "Gene expression in human neutrophils." Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317206.
Full textSavill, John Stewart. "Macrophage recognition of senescent neutrophils." Thesis, Imperial College London, 1989. http://hdl.handle.net/10044/1/47641.
Full textLiu, Li. "Complement and neutrophil activation on protein coated solid surfaces." Göteborg : Dept. of General and Marine Microbiology and Dept of medical Microbiology and Immunology, University of Göteborg, 1997. http://catalog.hathitrust.org/api/volumes/oclc/38986844.html.
Full textBordignon, Milena. "Relationship between AOPP (Advanced Oxidation Protein Products) and bovine neutrophils "in vitro": AOPP production by neutrophils and AOPP effects on neutrophils ROS production and viability." Doctoral thesis, Università degli studi di Padova, 2013. http://hdl.handle.net/11577/3422657.
Full textLo scopo del presente studio è stato quello di valutare le relazioni tra AOPP (prodotti avanzati di ossidazione proteica) e i neutrofili di bovino "in vitro". A questo scopo le AOPP sono state generate "in vitro", ossidando l'albumina sierica bovina con HOCl (acido ipocloroso) mentre i neutrofili di bovino sono stati isolati da sangue intero di bovine da latte. Le AOPP-BSA sono state incubate con i neutrofili di bovino appena isolati in condizioni di assenza di stimolo o stimolati con PMA un forte attivatore del "burst" respiratorio. La produzione di ROS da parte dei neutrofili e la loro vitalità , sono state misurate rispettivamente mediante chemiluminescenza amplificata dal luminolo e dai saggi MTT e lattato deidrogenasi (LDH). I risultati ottenuti hanno mostrato che le AOPP-BSA sono in grado di ridurre significativamente la produzione di ROS da parte dei neutrofili stimolati con PMA e la loro vitalità , misurata con il saggio MTT mentre non è stata rilevata lisi cellulare mediante saggio LDH. Sulla base di questi risultati il presente lavoro si è proposto di studiare se le AOPP sono in grado di scatenare eventi apopotici. A questo scopo le caspasi 3, 8 , 9 e la frammentazione del DNA sono stati utilizzati come marker con l'obiettivo di discriminare tra la via intrinseca e quella estrinseca di apoptosi. I risultati ottenuti hanno mostrato che i neutrofili di bovino non stimolati e incubati con AOPP-BSA per 1 ora e 6 ore, presentano una maggiore ma non significativa produzione di caspasi 8 attiva, se comparati con l'incubazione con BSA. Anche la caspasi 3 mosta un incremento, non significativo in neutrofili non stimolati incubati con AOPP-BSA per 6 ore, rispetto all'incubazione con BSA. Non è stata ottenuta alcuna differenza per quanto riguarda la caspasi 9 e la frammentazione del DNA. Tuttavia, in queste condizioni sperimentali è possibile concludere che la via intrinseca dell'apoptosi non è coinvolta nella riduszione della funzionalità dei neutrofili di bovino o nella loro vitalità ma i neutrofili di bovino incubati con AOPP-BSA sembrano piuttosto essere 'accompagnati' verso le fasi precoci della via estrinseca dell'apoptosi. Inoltre, il seguente studio ha voluto valutare la capacità dei neutrofili di bovino attivati di generare AOPP 'in vitro'. La BSA è stata incubata con neutrofili di bovino non stimolati e stimolati con PMA per 1-2-3 ore, ed è stata misurata la formazione di specifici marcatori di ossidazione proteica come le AOPP le ditirosine e i carbonili. La BSA incubata con neutrofili stimolati con PMA, presenta un livello significativamente alto di AOPP e ditirosine rispetto all'incubazione con neutrofili non stimolati. I carbonili invece sembrano non essere prodotti in queste condizioni, almeno nelle fasi inziali dell'incubazione. In parallelo, la BSA incubata con la stessa concentrazione di HOCl prodotta dai neutrofili stimolati, per 1-2-3 ore, presenta livelli più elevato di AOPP, ditirosine e carbonili. Tuttavia è possibile concludere che i neutrofili di bovino sono in grado di ossidare la BSA e generare modificazioni chimiche e strutturali come AOPP e ditirosine nelle condizioni sperimentate. I carbonili invece sembrano non essere un marcatore specifico di ossidazione proteica mediata dai neutrofili. In aggiunta la diretta esposizione della BSA all'HOCl non è in grado di mimare completamente la complessità degli eventi che portano all'ossidazione della BSA e alla produzione di AOPP da parte dei neutrofili attivati.
Koch, Crystal C. "Effects of azithromycin on human neutrophils." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ48018.pdf.
Full textNaylor, Emma J. "Interactions of neutrophils with Haemophilus influenzae." Thesis, University of Liverpool, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427016.
Full textMedeiros, Kyle Andrew. "Hypoxia and the activity of neutrophils." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12516.
Full textPolymorphonuclear leukocytes (neutrophils) play a major role in fighting off invading bacteria. They are the first of the inflammatory cells to migrate to sites of inflammation through a process known as chemotaxis. Neutrophils eliminate invading organisms is by phagocytosis. Each phagocytic event results in the accumulation of reactive oxygen species such as the superoxide. Under hypoxic conditions associated with inflammation at local tissues, a set of transcription factors known as hypoxia-inducible factors are activated. This family of transcription factors consists primarily of two members, hypoxia inducible factor-1 (HIF-1) and hypoxia inducible factor-2 (HIF-2). HIF-1 is a heterodimer composed of alpha and beta subsets. In this study, we examined the expression of HIF-1α, HIF-1β and HIF-2 in neutrophils under hypoxic conditions at different time intervals. Expression of HIF -1α significantly increased under hypoxic conditions as compared to the normoxia. The results provide evidence suggesting that HIF-1α is the primary factor in mediating oxygen homeostasis under hypoxic conditions by regulating superoxide generation in neutrophils.
Lowe, David. "The roles of neutrophils in tuberculosis." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/24828.
Full textWan, Shek-kong Thomas. "Neutrophil function tests in Chinese newborn infants." Hong Kong : University of Hong Kong, 1991. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13186292.
Full textMcColl, Shaun Reuss. "Factors affecting the regulation of leukotriene production by neutrophils." Title page, contents and summary only, 1987. http://web4.library.adelaide.edu.au/theses/09PH/09phm1288.pdf.
Full textRomanelli, Raquel G. "Activation of neutrophil collagenase in periodontitis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0022/MQ40756.pdf.
Full textRigby, David Andrew. "Inflammation-induced migration of neutrophils across the lymphatic endothelium." Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.561107.
Full textLaurans, Salomé. "Interactions neutrophiles-adénovirus : mécanismes moléculaires impliqués et rôle physiologique." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL030.
Full textPolynuclear neutrophils (PN) are innate immune cells, forming the first line of immune defense against pathogens. While their role in defense against bacteria and fungi is well known, their interactions with viruses have been less studied. During viral infections, PN may be either necessary for the infection resolution (HSV-1 or Influenza A Virus infections) or excessively recruited and/or activated, thus generating important damages to host tissues (Respiratory Syncytial Virus & SARS-CoV-2 infections). Among the viruses met by PN, adenoviruses (Ad) are responsible for mild infections. However, some serotypes can cause gastroenteritis epidemics, upper respiratory tract infections and, more recently, provoked a hepatitis epidemic among children. Very few studies have explored the interactions between PN and Ad. The aim of this work is therefore to better understand the consequences of these interactions on Ad and PN.Our study showed that Ad binding to human PN requires immunoglobulin G-opsonized Ad, which are then recognized by the CD32/FcγRIIa receptor. Moreover, using confocal and transmission electron microscopies, we observed Ad internalization as clusters within a phagosomal compartment. The PN-Ad interaction is associated with a rapid cytosolic calcium concentration increase that depends of the extracellular calcium. Moreover, Ad internalization triggers the reactive oxygen species (ROS) production, detected by chemiluminescence and an in-situ fluorescence probe, consistent with the recruitment of the cytosolic p67phox subunit of NADPH oxidase NOX2 to the Ad-containing phagosome. Ad internalization also leads after a few hours to rapid PN cell death through a lysis process that involves RIPK3 protein, one of the necroptosis actors, and calcium, but also Neutrophil Extracellular Traps (NET) formation. This death is, however, independent of NOX2 activation. Single-cell transcriptomics analysis indicates that Ad internalization induces transcription of specific genes in PN, including the one coding for IL-8. PN-Ad interaction also triggers ROS-independent but RIPK3 dependent IL-8 release but no significant leukotriene β4 secretion was observed. Moreover, at the multiplicity of infection tested, internalized Ad are not destroyed by phagocytosis and keep their infectious capacity.These data show that PN recognize opsonized Ad, internalize them and activate a specific transcriptional program. Moreover, PN exposed to Ad release ROS, IL-8 and NETs which accompany their lysis. This pro-inflammatory context could have consequences for the anti-adenoviral adaptive immune response
De, Chiara Alessia. "Molecular analysis of the prosurvival effect of cytosolic Proliferating Cell Nuclear Antigen (PCNA) in neutrophils." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05S002.
Full textPolymorphonuclear neutrophils (PMN), key cells of innate immunity are the first cell recruited to the inflammatory site. After destroying the pathogen, neutrophils undergo apoptosis and are cleared by macrophages to prevent the spillage of their lytic content that is dangerous for the environment. The regulation of the survival/apoptosis balance of neutrophil is a crucial step in the inflammation resolution. Our laboratory has shown the presence of Proliferating Cell Nuclear Antigen (PCNA) in mature neutrophils. PCNA is expressed in the nucleus of proliferating cells, where it is involved in DNA replication/repair and in cell cycle control. PCNA is a trimeric protein conserved during evolution and deprived of enzymatic activity. Indeed, PCNA is a “platform” that interacts with different partner proteins and orchestrates their functions. Furthermore, PCNA must be in trimeric form to play its role. In mature neutrophils, PCNA has an exclusively cytosolic localization where it specifically controls their survival. The PCNA translocation from nucleus to the cytosol happened during the granulocytic differentiation. This nuclear-to-cytosol relocalisation is dependent on a nuclear export sequence (NES), which is accessible and functional when PCNA is monomeric. The aim of my thesis was to study the PCNA platform in the neutrophil cytosol to identify the proteins associated with PCNA in order to understand its function in neutrophils. We have shown the expression of monomeric and trimeric forms of PCNA in the cytosol of mature neutrophils. We have demonstrated the anti-apoptotic activity of the monomeric form in PLB985 cells differentiated in neutrophils. Moreover, we have identified the surface-exposed peptides from the monomeric PCNA which are used as competitors of interactions between PCNA and its partner in the cytosol of neutrophils. These peptides modulate neutrophils survival. Thanks to the analysis of Mass Spectrometry, we have identified new partners of PCNA in the neutrophil cytosol involved in several metabolic pathways. This suggests that PCNA regulates neutrophil survival by interacting with different cytosolic proteins. Among the identified partners, we have found the cytosolic subunits of the NADPH oxidase, the enzyme responsible of the reactive oxygen species production, at the base of the neutrophil microbicidal activity. We have shown especially the interaction between p47phox and PCNA. Finally, we have investigated the functional implication of the interaction of PCNA with the NADPH oxidase in PLB985 cells and also in human neutrophils. Taken altogether, results suggest that the cytosolic PCNA maintains the resting state of neutrophils, and it helps the assembly of the NADPH oxidase when activated. The protein network associated with PCNA regulates the activity and the survival of neutrophil by modulating several pathways
Lawson, Roderick A. "Neutrophils in bacterial pneumonia : influx and clearance." Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/28407.
Full textBrumell, John H. "Phosphorylation-dependent signalling mechanisms in human neutrophils." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0018/NQ27612.pdf.
Full textReinhardt, P. Hans. "The function of VLA-4 on neutrophils." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0024/MQ31370.pdf.
Full textPerskvist, Nasrin. "Interaction between Mycobacterium tuberculosis and human neutrophils /." Linköping : Univ, 2001. http://www.bibl.liu.se/liupubl/disp/disp2001/med679s.pdf.
Full textHarris, Fiona Elizabeth. "The role of neutrophils in experimental vasculitis." Thesis, St George's, University of London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407971.
Full textPrigmore, Elena. "Rho family binding proteins in human neutrophils." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314081.
Full textPerry, Frances. "Oxidative responses of neutrophils to Streptococcus pneumoniae." Thesis, University of Bristol, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335509.
Full textFreitas, Marisa Andreia Carvalho de. "The Effect of Metals on Human Neutrophils." Doctoral thesis, Faculdade de Farmácia da Universidade do Porto, 2009. http://hdl.handle.net/10216/63815.
Full textCorleis, Bjoern. "Interaction of human neutrophils with mycobacterium tuberculosis." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.549780.
Full textCropp, Amy Rena. "Interaction of Bovine Seminal Proteins with Neutrophils." Thesis, The University of Arizona, 2006. http://hdl.handle.net/10150/193318.
Full textLaight, David W. "Neutrophils and vascular reactivity in ischaemia/reperfusion." Thesis, University of Bath, 1994. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385291.
Full textFreitas, Marisa Andreia Carvalho de. "The Effect of Metals on Human Neutrophils." Tese, Faculdade de Farmácia da Universidade do Porto, 2009. http://hdl.handle.net/10216/63815.
Full textKalupov, Timofey. "Protéases à serine du neutrophile et inflammations pulmonaires : 1. L’air exhalé condensé est-il un matériel adapté pour les mesures d’activités protéolytiques ? : 2. La spécificité des protéases neutrophiliques valide-t-elle l’utilisation du modèle souris de Broncho-Pneumopathie Chronique Obstructive (BPCO) ?" Thesis, Tours, 2009. http://www.theses.fr/2009TOUR3301/document.
Full textNeutrophils recruitment is a hallmark of the inflammation associated with different lung diseases. This recruitment leads to the release in the extracellular matrix of serine proteases that are responsible at least in part, of the degradation of the pulmonary tissue and/or of the chronicity of inflammation. The initial objective of this thesis was to develop a method of quantification of these proteases, based on the analysis of exhaled air condensate. But in spite of the sensitivity of the methods, we have not been able to detect any significant activity of neutrophil serine proteases in these condensates. This negative result however gave support a hypothesis we formulated on the extracellular biodistribution of proteases in lung secretions. The second part of this thesis was devoted to the validation of an animal model of chronic obstructive pulmonary disease, i.e. the mouse exposed to cigarette smoke. We have purified three murine serine neutrophil proteases and developed new sensitive and specific FRET substrates which were designed starting from molecular modeling studies. These new tools that validate the use of the mouse model of human COPD, will be of great help to understand the role of serine proteases for generating chemotactic peptides during this chronic disease
Schroder, Angie Lisa. "A Role for Neutrophil Extracellular Traps in the Pathogenesis of Inflammatory Bowel Disease." Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/28779.
Full textKoehl, Bérengère. "Implication de l'endotheline-1 dans l'adhérence et l'activation des polynucléaires neutrophiles dans la drépanocytose." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC112/document.
Full textSickle cell disease is a genetic disorder affecting red blood cells, due to a point mutation in the β chain of the hemoglobin gene. However, the pathophysiology of the disease goes well beyond the erythrocyte abnormalities, including vascular and white blood cell dysfunctions that contribute to the complexity of the disease. In this project, we investigated the role of endothelin-1, a powerful vasoconstrictor peptide involved in many vascular diseases, on activation and adhesion of neutrophil in sickle cell disease.We worked on both a mouse model of sickle cell disease (SAD mice) and blood samples from patients. In mice, we performed intravital microscopy experiments, to test the in vivo effect of endothelin receptor antagonists ETA and ETB on neutrophils recruitment. On blood samples from patients with sickle cell disease, we tested in vitro adhesion of neutrophils to vascular endothelium in response to the blocking of ETA and ETB receptors. Finally, we studied the expression of ETA and ETB receptors on neutrophils and the signaling pathways resulting in their activation.In our mouse model of sickle cell disease, the inhibition of both endothelin receptors ETA and ETB limits the major leukocyte recruitment caused by an inflammatory stimulus. These results confirm the role of ETA and the more unexpected important role of ETB in all stages of neutrophil adhesion and transmigration in sickle cell context.On human samples, we demonstrated the crucial role of ETB in neutrophils adhesion. We also confirmed the expression of ETA and ETB receptors on neutrophils. ETB receptor activates a signaling pathway responsible for intracytoplasmic calcium mobilization, but not involving the activation of phosphoinositide 3-kinase. Finally, we have shown the ability of neutrophils to synthesize and secrete endothelin-1, which can contribute to sustain the inflammatory stimulation and increased leukocyte recruitment.In conclusion, our work has highlighted the important role of ETB receptor in the recruitment of neutrophils in sickle cell disease. These data suggest that the antagonists of endothelin could be beneficial in prevention of vaso-occlusive events in sickle cell patients
Tam, Wai-kin, and 譚偉健. "A small scale study evaluating allelic frequencies of human neutrophil antigens in Hong Kong Chinese population." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206588.
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Summers, Charlotte. "Neutrophil priming : effects on pulmonary transit time and bio-distribution in vivo." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609579.
Full textROCK, JOHN PATRICK. "MOLECULAR BIOLOGY OF GONOCOCCAL DEATH FOLLOWING EXPOSURE TO THE GRANULE EXTRACTS OF HUMAN NEUTROPHILS (NEISSERIA GONORRHOEAE, PEPTIDOGLYCAN, MEMBRANE DAMAGE)." Diss., The University of Arizona, 1986. http://hdl.handle.net/10150/183844.
Full textIshak, Reezal. "Calpain-1 : investigating its role in murine neutrophils." Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/37448/.
Full textMorton, Jonathan. "Modulation of vascular tone by neutrophils in vivo." Thesis, Cardiff University, 2007. http://orca.cf.ac.uk/55681/.
Full textAdams, Susan. "Activated gene expression by neutrophils in rheumatoid arthritis." Thesis, University of Liverpool, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386829.
Full textStringer, Rebecca Elizabeth. "Endogenous and activated protein synthesis in human neutrophils." Thesis, University of Liverpool, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386847.
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