Littérature scientifique sur le sujet « Neutrophils »
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Articles de revues sur le sujet "Neutrophils"
Forlow, S. Bradley, Jill R. Schurr, Jay K. Kolls, Gregory J. Bagby, Paul O. Schwarzenberger et Klaus Ley. « Increased granulopoiesis through interleukin-17 and granulocyte colony-stimulating factor in leukocyte adhesion molecule–deficient mice ». Blood 98, no 12 (1 décembre 2001) : 3309–14. http://dx.doi.org/10.1182/blood.v98.12.3309.
Texte intégralMcGovern, Toby K., Michael Chen, Benoit Allard, Kjell Larsson, James G. Martin et Mikael Adner. « Neutrophilic oxidative stress mediates organic dust-induced pulmonary inflammation and airway hyperresponsiveness ». American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no 2 (15 janvier 2016) : L155—L165. http://dx.doi.org/10.1152/ajplung.00172.2015.
Texte intégralYamasaki, Akira, Ryota Okazaki et Tomoya Harada. « Neutrophils and Asthma ». Diagnostics 12, no 5 (8 mai 2022) : 1175. http://dx.doi.org/10.3390/diagnostics12051175.
Texte intégralMizgerd, J. P., B. B. Meek, G. J. Kutkoski, D. C. Bullard, A. L. Beaudet et C. M. Doerschuk. « Selectins and neutrophil traffic : margination and Streptococcus pneumoniae-induced emigration in murine lungs. » Journal of Experimental Medicine 184, no 2 (1 août 1996) : 639–45. http://dx.doi.org/10.1084/jem.184.2.639.
Texte intégralWeinmann, Pamela, Karin Scharffetter-Kochanek, S. Bradley Forlow, Thorsten Peters et Barbara Walzog. « A role for apoptosis in the control of neutrophil homeostasis in the circulation : insights from CD18-deficient mice ». Blood 101, no 2 (15 janvier 2003) : 739–46. http://dx.doi.org/10.1182/blood-2002-01-0239.
Texte intégralBorges, Leandro, Tania Cristina Pithon-Curi, Rui Curi et Elaine Hatanaka. « COVID-19 and Neutrophils : The Relationship between Hyperinflammation and Neutrophil Extracellular Traps ». Mediators of Inflammation 2020 (2 décembre 2020) : 1–7. http://dx.doi.org/10.1155/2020/8829674.
Texte intégralWang, Guoshun, et Hang Pong Ng. « Myeloid CFTR Loss-of-function Causes Persistent Neutrophilic Inflammation in Cystic Fibrosis ». Journal of Immunology 202, no 1_Supplement (1 mai 2019) : 187.33. http://dx.doi.org/10.4049/jimmunol.202.supp.187.33.
Texte intégralTomar, Bhawna, Hans-Joachim Anders, Jyaysi Desai et Shrikant R. Mulay. « Neutrophils and Neutrophil Extracellular Traps Drive Necroinflammation in COVID-19 ». Cells 9, no 6 (2 juin 2020) : 1383. http://dx.doi.org/10.3390/cells9061383.
Texte intégralInauen, W., D. N. Granger, C. J. Meininger, M. E. Schelling, H. J. Granger et P. R. Kvietys. « Anoxia-reoxygenation-induced, neutrophil-mediated endothelial cell injury : role of elastase ». American Journal of Physiology-Heart and Circulatory Physiology 259, no 3 (1 septembre 1990) : H925—H931. http://dx.doi.org/10.1152/ajpheart.1990.259.3.h925.
Texte intégralGadjeva, Mihaela, Abirami Kugadas, Anastasia Petenkova, Jennifer Geddes-McAlister, Michael K. Mansour et David Sykes. « Neutrophil maturation and their response to infectious pathogens are regulated by microbiota ». Journal of Immunology 202, no 1_Supplement (1 mai 2019) : 127.22. http://dx.doi.org/10.4049/jimmunol.202.supp.127.22.
Texte intégralThèses sur le sujet "Neutrophils"
Gillis, Caitlin. « Neutrophils in IgG- and endotoxin-induced systemic inflammation : protective or pathological agents ? » Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066279/document.
Texte intégralNeutrophils 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
Mawhin, Marie-Anne. « Role of neutrophils and leukotrienes in atherosclerotic plaque destabilisation : implication of endotoxemia ». Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ034/document.
Texte intégralAtherosclerotic 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.
Texte intégralManriquez, 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.
Texte intégralNeisseria 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.
Texte intégralGRIMOLIZZI, 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.
Texte intégralHuman 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.
Texte intégralHemostasis 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.
Texte intégralCross, Andrew. « Molecular properties of inflammatory neutrophils ». Thesis, University of Liverpool, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250467.
Texte intégralMacLeod, Ronald. « Gene expression in human neutrophils ». Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317206.
Texte intégralLivres sur le sujet "Neutrophils"
S, Abramson Jon, et Wheeler J. Gary, dir. The Neutrophil. Oxford : IRL Press at Oxford University Press, 1993.
Trouver le texte intégralTuominen-Gustafsson, Helena Birgitta. Calcium signalling pathways in human neutrophils. Åbo : Åbo Akademis Förlag, 1998.
Trouver le texte intégralAlonso-Fernández, Patricia. Neutrophils in biological age and longevity. New York : Nova Science Publishers, Inc., 2011.
Trouver le texte intégralI, Gabrilovich Dmitry, dir. The neutrophils : New outlook for old cells. 2e éd. Hackensack, N.J : Imperial College Press, 2004.
Trouver le texte intégral1952-, Hallett Maurice B., dir. The Neutrophil : Cellular biochemistry and physiology. Boca Raton, Fla : CRC Press, 1989.
Trouver le texte intégralHallett, Maurice B. The molecular and ionic signalling of neutrophils. New York : Chapman & Hall, 1997.
Trouver le texte intégralBrumell, John H. Phosphorylation-dependent signalling mechanisms in human neutrophils. Ottawa : National Library of Canada = Bibliothèque nationale du Canada, 1997.
Trouver le texte intégralHallett, Maurice B. The molecular and ionic signaling of neutrophils. Austin. Tex : Landes Bioscience, 1997.
Trouver le texte intégralDeFranco, Jamie E. Neutrophils : Lifespan, functions, and roles in disease. Hauppauge, N.Y : Nova Science, 2010.
Trouver le texte intégralHerbold, Ralf. Ex-vivo Generierung von neutrophilen Zellen zur Prävention und Therapie der Sepsis. Jülich : Forschungszentrum Jülich, Zentralbibliothek, 2005.
Trouver le texte intégralChapitres de livres sur le sujet "Neutrophils"
Whyte, Moira. « Neutrophils ». Dans Cellular Mechanisms in Airways Inflammation, 125–46. Basel : Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8476-1_4.
Texte intégralZurier, Robert B. « Neutrophils ». Dans Encyclopedia of Medical Immunology, 774–77. New York, NY : Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_23.
Texte intégralCuzzocrea, Salvatore. « Neutrophils ». Dans Inflammation - From Molecular and Cellular Mechanisms to the Clinic, 253–72. Weinheim, Germany : Wiley-VCH Verlag GmbH & Co. KGaA, 2017. http://dx.doi.org/10.1002/9783527692156.ch10.
Texte intégralJain, Rohit, Andrew J. Mitchell, Szun S. Tay, Ben Roediger et Wolfgang Weninger. « Neutrophils ». Dans Immunology of the Skin, 147–67. Tokyo : Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55855-2_9.
Texte intégralClausen, Torben, José Luis Trejo, Mark P. Mattson, Alexis M. Stranahan, Joanna Erion, Rosa Maria Bruno, Stefano Taddei et Melinda M. Manore. « Neutrophils ». Dans Encyclopedia of Exercise Medicine in Health and Disease, 644. Berlin, Heidelberg : Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2760.
Texte intégralGevaert, Elien. « Neutrophils ». Dans Chronic Rhinosinusitis, 69–79. Singapore : Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-0784-4_9.
Texte intégralZweiman, Burton. « Neutrophils ». Dans Inflammatory Mechanisms in Allergic Diseases, 77–95. Boca Raton : CRC Press, 2023. http://dx.doi.org/10.1201/9780429134432-6.
Texte intégralKuijpers, Taco W., Timo K. van den Berg et Dirk Roos. « Neutrophils Forever … ». Dans Phagocyte-Pathogen Interactions, 1–26. Washington, DC, USA : ASM Press, 2014. http://dx.doi.org/10.1128/9781555816650.ch1.
Texte intégralOliveira, André Gustavo, Rodrigo Guabiraba, Mauro Martins Teixeira et Gustavo Batista Menezes. « Tumor-Associated Neutrophils ». Dans Trends in Stem Cell Proliferation and Cancer Research, 479–501. Dordrecht : Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6211-4_18.
Texte intégralLeino, Lasse. « Chemotaxis of Neutrophils ». Dans Encyclopedia of Immunotoxicology, 176–78. Berlin, Heidelberg : Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_251.
Texte intégralActes de conférences sur le sujet "Neutrophils"
Selak, M. A., M. Chignard et J. B. Smith. « CHARACTERIZATION OF A NEUTROPHIL CPYMOTRYPSIN-LIKE ENZYME THAT ACTIVATES PLATELETS ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643157.
Texte intégralTeo, Soo Kng, Kim H. Parker et K. H. Chiam. « Viscoelastic Finite-Element Modelling of Neutrophil Deformation in a Tapered Micropipette ». Dans ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-191099.
Texte intégralSounbuli, K., N. L. Mironova, O. V. Markov et L. A. Alekseeva. « A COMPARATIVE STUDY OF DIFFERENT ISOLATION PROTOCOLS OF MURINE NEUTROPHILS FROM BONE MARROW AND SPLEEN ». Dans OpenBio-2023. ИПЦ НГУ, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-52.
Texte intégralMarcus, A. J., L. B. Safier, H. L. Ullman, N. Islam, M. J. Broekman et C. V. Schacky. « NEW EICOSANOIDS FORMED DURING PLATELET-NEUTROPHIL INTERACTIONS ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644626.
Texte intégralCoeffier, E., D. Joseph et B. B. Vargaftio. « PLATELET-LEUKOCYTE INTERACTION : ACTIVATION OF RABBIT PLATELETS BY FMLP-STIMULATED NEUTROPHILS ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643158.
Texte intégralBell, D., M. Jackson, C. MacRae, A. L. Muir et J. Dawes. « NEUTROPHIL ELASTASE IS A MARKER OF NEUTROPHIL ACTIVATION IN ACUTE MYOCARDIAL INFARCTION ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643020.
Texte intégralMuylle, L., C. Van Brussel, D. R. van Bockstaele et M. E. Peetermans. « IN VITRO NEUTROPHIL ACTIVATION BY PLASMA OF STORED PLATELET CONCENTRATES ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644686.
Texte intégralFarache Trajano, Luiza, Rebecca Moore et Quentin Sattentau. « The Presence of Chemical Cross-Linking Stabilises HIV-1 Envelope Glycoprotein Trimer Antigens in a Model of Intramuscular Immunisation ». Dans Building Bridges in Medical Science 2021. Cambridge Medicine Journal, 2021. http://dx.doi.org/10.7244/cmj.2021.03.001.4.
Texte intégralAlteraifi, Abdullatif M., et Doncho V. Zhelev. « Cytoskeleton Rearrangement in Activated Human Neutrophils ». Dans ASME 1996 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1996. http://dx.doi.org/10.1115/imece1996-1110.
Texte intégralShirai, A., et T. Hayase. « Effect of Retention Time of Neutrophils in Alveolar Capillaries on Increase in Their Concentration in the Capillary Network ». Dans ASME/JSME 2007 5th Joint Fluids Engineering Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/fedsm2007-37653.
Texte intégralRapports d'organisations sur le sujet "Neutrophils"
Boston, Mark E. Effects of Nasal Saline Spray on Human Neutrophils. Fort Belvoir, VA : Defense Technical Information Center, septembre 2002. http://dx.doi.org/10.21236/ada406691.
Texte intégralLiang, Feixin. Progress in Liquid Biopsy : A possible role of neutrophils. Science Repository, août 2018. http://dx.doi.org/10.31487/j.cor.2018.02.004.
Texte intégralViksna, Ludmila, Oksana Kolesova, Aleksandrs Kolesovs, Ieva Vanaga et Seda Arutjunana. Clinical characteristics of COVID-19 patients (Latvia, Spring 2020). Rīga Stradiņš University, décembre 2020. http://dx.doi.org/10.25143/fk2/hnmlhh.
Texte intégralBoston, Mark E., G. C. Frech, Enrique Chacon-Cruz, E. S. Buescher et David G. Oelberg. Surfactant Releases Internal Calcium Stores in Neutrophils by G Protein-Mediated Pathway. Fort Belvoir, VA : Defense Technical Information Center, octobre 2002. http://dx.doi.org/10.21236/ada413640.
Texte intégralHaight, Gary. Inquiry into the causes and significance of cytoplasmic vacuolation of neutrophils in the peripheral circulation. Portland State University Library, janvier 2000. http://dx.doi.org/10.15760/etd.5283.
Texte intégralYoungman, Sara. The Chemotactic Response of Neutrophils to Components of the Sera of Mice Infected with Trichinella spiralis. Portland State University Library, janvier 2000. http://dx.doi.org/10.15760/etd.6942.
Texte intégralBowles, Charles A., et Andrew Baum. Investigation of Stress Induced Alterations in Neutrophil Function. Fort Belvoir, VA : Defense Technical Information Center, mai 1991. http://dx.doi.org/10.21236/ada237002.
Texte intégralTrofimenko, A., M. Mamus, S. Bedina, E. Mozgovaya et S. Spitsina. PARTICIPATION OF NEUTROPHIL EXTRACELLULAR TRAPS IN AUTOIMMUNE RHEUMATIC DISEASES. DOI CODE, 2021. http://dx.doi.org/10.18411/wco-iof-esceo-2021-509.
Texte intégralBechev, Blagovest, Moni Magrisso, Stilian Stoeff et Pavlina Glogovska. Possible Application in Pulmonology of Neutrophil Population Functional State Evaluated by Chemiluminescent Method. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, mars 2019. http://dx.doi.org/10.7546/crabs.2019.03.15.
Texte intégralGoldman, Gideon, Richard Welbourn, C. R. aleri, David Shepro et Herbert B. Hechtman. Leukotriene B4 and Thromboxane A2 are Essential Cofactors in CD 18 Dependent Neutrophil Diapedesis. Fort Belvoir, VA : Defense Technical Information Center, juillet 1990. http://dx.doi.org/10.21236/ada360180.
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