Academic literature on the topic 'Neutrophils'
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Journal articles on the topic "Neutrophils"
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Forlow, S. Bradley, Jill R. Schurr, Jay K. Kolls, Gregory J. Bagby, Paul O. Schwarzenberger, and Klaus Ley. "Increased granulopoiesis through interleukin-17 and granulocyte colony-stimulating factor in leukocyte adhesion molecule–deficient mice." Blood 98, no. 12 (December 1, 2001): 3309–14. http://dx.doi.org/10.1182/blood.v98.12.3309.
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Abstract Many mutant mice deficient in leukocyte adhesion molecules display altered hematopoiesis and neutrophilia. This study investigated whether peripheral blood neutrophil concentrations in these mice are elevated as a result of accumulation of neutrophils in the circulation or altered hematopoiesis mediated by a disrupted regulatory feedback loop. Chimeric mice were generated by transplanting various ratios of CD18+/+ and CD18−/− unfractionated bone marrow cells into lethally irradiated wild-type mice, resulting in approximately 0%, 10%, 50%, 90%, or 100% CD18 null neutrophils in the blood. The presence of only 10% CD18+/+ neutrophils was sufficient to prevent the severe neutrophilia seen in mice reconstituted with CD18−/− bone marrow cells. These data show that the neutrophilia in CD18−/− mice is not caused by enhanced neutrophil survival or the inability of neutrophils to leave the vascular compartment. In CD18−/−, CD18−/−E−/−, CD18−/−P−/−, EP−/−, and EPI−/− mice, levels of granulocyte colony-stimulating factor (G-CSF) and interleukin-17 (IL-17) were elevated in proportion to the neutrophilia seen in these mice, regardless of the underlying mutation. Antibiotic treatment or the propensity to develop skin lesions did not correlate with neutrophil counts. Blocking IL-17 or G-CSF function in vivo significantly reduced neutrophil counts in severely neutrophilic mice by approximately 50% (P < .05) or 70% (P < .01), respectively. These data show that peripheral blood neutrophil numbers are regulated by a feedback loop involving G-CSF and IL-17 and that this feedback loop is disrupted when neutrophils cannot migrate into peripheral tissues.
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McGovern, Toby K., Michael Chen, Benoit Allard, Kjell Larsson, James G. Martin, and 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 (January 15, 2016): L155—L165. http://dx.doi.org/10.1152/ajplung.00172.2015.
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Airway exposure to organic dust (OD) from swine confinement facilities induces airway inflammation dominated by neutrophils and airway hyperresponsiveness (AHR). One important neutrophilic innate defense mechanism is the induction of oxidative stress. Therefore, we hypothesized that neutrophils exacerbate airway dysfunction following OD exposure by increasing oxidant burden. BALB/C mice were given intranasal challenges with OD or PBS (1/day for 3 days). Mice were untreated or treated with a neutrophil-depleting antibody, anti-Ly6G, or the antioxidant dimethylthiourea (DMTU) prior to OD exposure. Twenty-four hours after the final exposure, we measured airway responsiveness in response to methacholine (MCh) and collected bronchoalveolar lavage fluid to assess pulmonary inflammation and total antioxidant capacity. Lung tissue was harvested to examine the effect of OD-induced antioxidant gene expression and the effect of anti-Ly6G or DMTU. OD exposure induced a dose-dependent increase of airway responsiveness, a neutrophilic pulmonary inflammation, and secretion of keratinocyte cytokine. Depletion of neutrophils reduced OD-induced AHR. DMTU prevented pulmonary inflammation involving macrophages and neutrophils. Neutrophil depletion and DMTU were highly effective in preventing OD-induced AHR affecting large, conducting airways and tissue elastance. OD induced an increase in total antioxidant capacity and mRNA levels of NRF-2-dependent antioxidant genes, effects that are prevented by administration of DMTU and neutrophil depletion. We conclude that an increase in oxidative stress and neutrophilia is critical in the induction of OD-induced AHR. Prevention of oxidative stress diminishes neutrophil influx and AHR, suggesting that mechanisms driving OD-induced AHR may be dependent on neutrophil-mediated oxidant pathways.
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Yamasaki, Akira, Ryota Okazaki, and Tomoya Harada. "Neutrophils and Asthma." Diagnostics 12, no. 5 (May 8, 2022): 1175. http://dx.doi.org/10.3390/diagnostics12051175.
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Although eosinophilic inflammation is characteristic of asthma pathogenesis, neutrophilic inflammation is also marked, and eosinophils and neutrophils can coexist in some cases. Based on the proportion of sputum cell differentiation, asthma is classified into eosinophilic asthma, neutrophilic asthma, neutrophilic and eosinophilic asthma, and paucigranulocytic asthma. Classification by bronchoalveolar lavage is also performed. Eosinophilic asthma accounts for most severe asthma cases, but neutrophilic asthma or a mixture of the two types can also present a severe phenotype. Biomarkers for the diagnosis of neutrophilic asthma include sputum neutrophils, blood neutrophils, chitinase-3-like protein, and hydrogen sulfide in sputum and serum. Thymic stromal lymphoprotein (TSLP)/T-helper 17 pathways, bacterial colonization/microbiome, neutrophil extracellular traps, and activation of nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 pathways are involved in the pathophysiology of neutrophilic asthma and coexistence of obesity, gastroesophageal reflux disease, and habitual cigarette smoking have been associated with its pathogenesis. Thus, targeting neutrophilic asthma is important. Smoking cessation, neutrophil-targeting treatments, and biologics have been tested as treatments for severe asthma, but most clinical studies have not focused on neutrophilic asthma. Phosphodiesterase inhibitors, anti-TSLP antibodies, azithromycin, and anti-cholinergic agents are promising drugs for neutrophilic asthma. However, clinical research targeting neutrophilic inflammation is required to elucidate the optimal treatment.
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Mizgerd, J. P., B. B. Meek, G. J. Kutkoski, D. C. Bullard, A. L. Beaudet, and C. M. Doerschuk. "Selectins and neutrophil traffic: margination and Streptococcus pneumoniae-induced emigration in murine lungs." Journal of Experimental Medicine 184, no. 2 (August 1, 1996): 639–45. http://dx.doi.org/10.1084/jem.184.2.639.
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The roles of selectins in the pulmonary margination and emigration of neutrophils were investigated by using mice genetically deficient in both E- and P-selectins (E/P mutants) and/or by intravenous injections of fucoidin (inhibiting both L- and P-selectins). E/P mutants were neutrophilic (14.7 +/- 4.9 x 10(6) vs. 0.8 +/- 0.1 x 10(6) neutrophils/ml). This neutrophilia was associated with increased margination of neutrophils within pulmonary capillaries (39.7 +/- 9.4 vs. 4.6 +/- 1.1 neutrophil profiles per 100 red blood cell profiles) but no change in margination within noncapillary pulmonary microvessels. After intratracheal instillation of Streptococcus pneumoniae, lungs of E/P mutants displayed increased neutrophil emigration (564 +/- 92 vs. 116 +/- 19 neutrophils per 100 alveolar profiles), edema (5.3 +/- 1.5 vs. 1.5 +/- 0.4 microliter/g body weight), and histologic evidence of lung injury compared with those in wild-type (WT). Fucoidin treatment did not affect neutrophil emigration during streptococcal pneumonia in WT or E/P mice. During pneumonia, the number of white blood cells (WBC) tethered to or spread upon the noncapillary vessel endothelium increased in both WT and E/P lungs. These are the first data demonstrating that neutrophil margination in uninfected pulmonary capillaries does not require E- and P-selectins; that streptococcal pneumonia induces an E- and P-selectin-independent increase in WBC interactions with noncapillary endothelium; and that migration of neutrophils to alveoli can occur despite deficiency or inhibition of all of the known selectins.
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Weinmann, Pamela, Karin Scharffetter-Kochanek, S. Bradley Forlow, Thorsten Peters, and Barbara Walzog. "A role for apoptosis in the control of neutrophil homeostasis in the circulation: insights from CD18-deficient mice." Blood 101, no. 2 (January 15, 2003): 739–46. http://dx.doi.org/10.1182/blood-2002-01-0239.
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The control of neutrophil turnover in the circulation is a key event in homeostasis and inflammation. Using CD18- deficient (CD18−/−) mice that show a 19-fold increase of blood neutrophil counts when compared with wild-type animals (CD18+/+), we found that apoptosis of peripheral neutrophils was significantly reduced from 27.4% in the wild-type to 4.8% inCD18−/− mice within 4 hours after isolation as measured by analysis of DNA content. This was confirmed by detecting CD16 expression, nuclear morphology, and internucleosomal DNA degradation. In contrast, no difference in apoptosis was observed in neutrophils derived from the bone marrow. Neutrophilia and delayed neutrophil apoptosis were also present inCD18−/−/interleukin 6 (IL-6−/−) double knockout mice. Moreover, plasma ofCD18−/− mice was not able to delay apoptosis of CD18+/+neutrophils and plasma ofCD18+/+ mice did not augment apoptosis of CD18−/−neutrophils. However,CD18−/− neutrophils revealed an up-regulation of the antiapoptotic gene bcl-Xl and a down-regulation of the proapoptotic gene bax-α compared withCD18+/+ neutrophils suggesting that this delayed apoptosis. Accordingly, down-regulation of Bax-α using antisense technique delayed apoptosis and prolonged neutrophil survival. The replacement of the hematopoietic system of CD18+/+ mice by a 1:1 mixture of CD18+/+ andCD18−/− hematopoietic cells abolished the delay of apoptosis in peripheralCD18−/− neutrophils and prevented neutrophilia. Altogether, this suggests that a delay of neutrophil apoptosis inCD18−/− mice causes an alteration of neutrophil homeostasis, which may induce the massive increase of peripheral neutrophil counts. Thus, apoptosis seems to be critically involved in the control of neutrophil turnover in the circulation.
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Borges, Leandro, Tania Cristina Pithon-Curi, Rui Curi, and Elaine Hatanaka. "COVID-19 and Neutrophils: The Relationship between Hyperinflammation and Neutrophil Extracellular Traps." Mediators of Inflammation 2020 (December 2, 2020): 1–7. http://dx.doi.org/10.1155/2020/8829674.
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Coronavirus disease 2019 (COVID-19) is a virus-induced respiratory disease that may progress to acute respiratory distress syndrome (ARDS) and is triggered by immunopathological mechanisms that cause excessive inflammation and leukocyte dysfunction. Neutrophils play a critical function in the clearance of bacteria with specific mechanisms to combat viruses. The aim of this review is to highlight the current advances in the pathways of neutrophilic inflammation against viral infection over the past ten years, focusing on the production of neutrophil extracellular traps (NETs) and its impact on severe lung diseases, such as COVID-19. We focused on studies regarding hyperinflammation, cytokine storms, neutrophil function, and viral infections. We discuss how the neutrophil’s role could influence COVID-19 symptoms in the interaction between hyperinflammation (overproduction of NETs and cytokines) and the clearance function of neutrophils to eliminate the viral infection. We also propose a more in-depth investigation into the neutrophil response mechanism targeting NETosis in the different phases of COVID-19.
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Wang, Guoshun, and Hang Pong Ng. "Myeloid CFTR Loss-of-function Causes Persistent Neutrophilic Inflammation in Cystic Fibrosis." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 187.33. http://dx.doi.org/10.4049/jimmunol.202.supp.187.33.
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Abstract Persistent neutrophilic inflammation is a hallmark manifestation of cystic fibrosis (CF). However, the mechanism underlying this phenomenal clinical symptom remains incompletely understood. Here we report a pivotal role of CFTR in myeloid immune cells in control of neutrophilic inflammation. Myeloid CFTR-Knockout (Mye-Cftr−/−) mice and Wild-type (WT) mice were challenged peritoneally with zymosan at different doses. The lethal-dose challenge resulted in significantly higher mortality in Mye-Cftr−/− mice, indicating an intrinsic defect in host protection against inflammation in CF. The sub-lethal-dose challenge demonstrated an impaired resolution of inflammation in Mye-Cftr−/− mice, reflected by persistent neutrophilic inflammation, and hyper-inflammation with significantly higher levels of pro-inflammatory cytokines, including the neutrophil-recruiting chemokines MIP-2 and KC, which led to excessive neutrophil recruitment in vivo. Pulmonary challenge with zymosan confirmed the peritoneal finding. To determine the major types of cells responsible for the over-recruitment of neutrophils, zymosan-elicited peritoneal neutrophils and macrophages from Mye-Cftr−/− and WT mice were FACS-sorted and cultured ex vivo. The CF neutrophils produced significantly more neutrophil chemokine MIP-2. Moreover, peripheral blood neutrophils and monocytes from Mye-Cftr−/− and WT mice were cultured and stimulated with zymosan in vitro. Similarly, the CF neutrophils produced significantly more MIP-2. These data altogether suggest that CFTR dysfunction in myeloid immune cells leads to excessive neutrophil recruitment, thus serving as a mechanism for the long-observed neutrophilic inflammation in CF.
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Tomar, Bhawna, Hans-Joachim Anders, Jyaysi Desai, and Shrikant R. Mulay. "Neutrophils and Neutrophil Extracellular Traps Drive Necroinflammation in COVID-19." Cells 9, no. 6 (June 2, 2020): 1383. http://dx.doi.org/10.3390/cells9061383.
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The COVID-19 pandemic is progressing worldwide with an alarming death toll. There is an urgent need for novel therapeutic strategies to combat potentially fatal complications. Distinctive clinical features of severe COVID-19 include acute respiratory distress syndrome, neutrophilia, and cytokine storm, along with severe inflammatory response syndrome or sepsis. Here, we propose the putative role of enhanced neutrophil infiltration and the release of neutrophil extracellular traps, complement activation and vascular thrombosis during necroinflammation in COVID-19. Furthermore, we discuss how neutrophilic inflammation contributes to the higher mortality of COVID-19 in patients with underlying co-morbidities such as diabetes and cardiovascular diseases. This perspective highlights neutrophils as a putative target for the immunopathologic complications of severely ill COVID-19 patients. Development of the novel therapeutic strategies targeting neutrophils may help reduce the overall disease fatality rate of COVID-19.
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Inauen, W., D. N. Granger, C. J. Meininger, M. E. Schelling, H. J. Granger, and 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 (September 1, 1990): H925—H931. http://dx.doi.org/10.1152/ajpheart.1990.259.3.h925.
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The aim of this study was to assess the role of neutrophilic elastase in anoxia-reoxygenation-induced, neutrophil-mediated injury to microvascular endothelium. Cultured bovine microvascular endothelial cells were grown to confluence and labeled with 51Cr. The endothelial cells were exposed to a 30-min period of anoxia and subsequently reoxygenated. Endothelial cell injury, quantitated as 51Cr release and cell detachment, was determined 8 h after reoxygenation. Addition of neutrophils upon reoxygenation enhanced the anoxia-reoxygenation-induced increase in 51Cr release and cell detachment. The neutrophil-mediated injury was associated with elastase release from the neutrophils. Four agents were used to inhibit neutrophilic elastase activity: Eglin C, methoxysuccunyl-Ala2-Pro-Val-CH2Cl, L658,758, and a monoclonal antibody against neutrophilic elastase. All elastase inhibitors attenuated the neutrophil-mediated endothelial cell detachment but not 51Cr release. Addition of purified human neutrophilic elastase, at a level that mimicked the release from neutrophils, increased cell detachment in endothelial cells exposed to anoxia-reoxygenation but did not affect 51Cr release. Our results indicate that elastase plays an important role in anoxia-reoxygenation-induced, neutrophil-mediated endothelial cell dysfunction.
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Gadjeva, Mihaela, Abirami Kugadas, Anastasia Petenkova, Jennifer Geddes-McAlister, Michael K. Mansour, and David Sykes. "Neutrophil maturation and their response to infectious pathogens are regulated by microbiota." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 127.22. http://dx.doi.org/10.4049/jimmunol.202.supp.127.22.
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Abstract It has long been considered that a neutrophil’s response to various infectious challenges is innately pre-determined. Here, we provide data that demonstrates that neutrophil proteomes are modulated by the microbiota. We found that the proteomic signatures of mature neutrophils derived from germ free (GF) and specific pathogen free (SPF) mice were significantly different. In the absence of microbiota, mature neutrophils lacked GM-CSF-driven priming. To identify molecular pathways, we set-up an in vitro system where neutrophil progenitors were transduced with lenti-guides to knock-down key microbiota-driven pathway gene targets. GF-serum exposed neutrophil progenitors did not mature efficiently and had compromised bactericidal properties when compared to progenitors matured in SPF-derived serum. To identify which of the microbiota-driven proteins directly impacted bactericidal functions of neutrophils, we knocked out 19 candidates and tested their killing efficacy. Among all tested clones, one demonstrated a superior inhibition of neutrophil’s bactericidal capacities. Excitingly, this protein had no previously identified function: the knock down of prenylcysteine oxidase-like 1 (pcyox 1l) protein reduced neutrophil’s ability to kill efficiently P. aeruginosa in vitro due to diminished ROS release. Hence, we identified a novel mechanism for microbiota-driven control of innate immunity. Cumulatively, the data support the concept that microbiota affects neutrophil maturation by defining not only the quantity, but also the quality of mature neutrophils. We predict that neutrophil responses can be specifically tailored to pathogens.
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.
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Les neutrophiles contribuent à l'inflammation protectrice et pathologique. Ce projet de thèse consiste à déterminer le rôle des neutrophiles dans des modèles d'inflammation systémique graves et potentiellement mortelles, induite par le lipopolysaccharide (LPS, endotoxémie) ou par des complexes immuns antigène-anticorps (anaphylaxie). L'anaphylaxie est une réaction allergique qui peut être IgE- et/ou IgG-dépendante. L’endotoxémie est un modèle pertinent de l'inflammation au cours de maladies graves. Pour étudier les neutrophiles in vivo, nous avons utilisé un nouveau modèle murin de neutropénie inductible. Nous montrons que les neutrophiles et la Myélopéroxidase qu’ils produisent ont un rôle protecteur dans le choc endotoxique, indépendamment de l'environnement microbiologique. A l'inverse, les neutrophiles peuvent contribuer à l'anaphylaxie induite par les IgG chez la souris. Comme les récepteurs pour les IgG (FcγR) murins sont très différents des humains, nous avons développé un modèle de souris knock-in dans lequel les FcγR murins a été remplacé par les FcγR humains, activateurs et inhibiteur. Chez ces souris, nous montrons que des IgG humaines peuvent induire une anaphylaxie: le FcγRIIA a un rôle dominant, via l'activation des neutrophiles, et les médiateurs PAF et histamine. En parallèle, nous développons un modèle murin d’anaphylaxie à un curare, le Rocuronium, utilisé en clinique. Au même temps, dans une étude clinique, les résultats d’analyses des échantillons sanguins des patients suspectés d’avoir subi une anaphylaxie au curare soutien notre hypothèse de travail: que l’activation des neutrophiles par des IgG spécifiques est impliquée dans l'anaphylaxie humaineNeutrophils 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
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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.
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Au cours des infections, les polynucléaires neutrophiles libèrent des Neutrophil Extracellular Traps (NETs) pour capturer les agents pathogènes et les détruire. Les NETs; en coordination avec les plaquettes et les cellules immunitaires, activent la coagulation et participent à l’immunothrombose pour piéger les agents pathogènes et éviter leur dissémination. Ils sont dégradés physiologiquement par les DNases et les macrophages. Exacerbée, les NETs sont responsables de dommages cellulaires et tissulaires. Ils sont décrits comme des acteurs centraux de nombreuses pathologies, notamment comme participant à la thrombose (artérielle et veineuse), et aux formes sévères de la COVID-19. Cependant, les techniques de dosages de NETs et des DNases ne sont à ce jour pas standardisés et les mécanismes sous-jacent à l’exacerbation de la NETose au cours de la COVID-19 peu décrits.Nous émettons l’hypothèse que l’aggravation clinique des patients au cours de la COVID-19 est liée à un déséquilibre entre les NETS et les DNases.Pour réponde à cette hypothèse, nous avons pour objectifs : (1) définir les conditions pré-analytiques optimales pour doser les marqueurs de NETs; (2) mettre au point et valider une méthode de dosage de l’activité des DNases plasmatiques ; (3) Évaluer la balance entre marqueurs de NETs et activité des DNases en fonction de la sévérité de la COVID-19 ; (4) Étudier les mécanismes responsables de ce déséquilibre NETs/DNases.Identifier déficit en DNase comme facteur aggravant chez les patents permettrait d’imaginer de nouvelles thérapeutiques innovantes pour prévenir cette aggravation clinique comme l’administration de DNaseNeutrophil 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
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Mawhin, Marie-Anne. "Role of neutrophils and leukotrienes in atherosclerotic plaque destabilisation : implication of endotoxemia." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ034/document.
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La déstabilisation de la plaque d’athérosclérose reste de nos jours un problème majeur, malgré les progrès récents dans sa compréhension. Les neutrophiles sont des acteurs puissants de l’immunité innée capables d’altérer les plaques. Un chimio-attractant majeur des neutrophiles, le leucotriène B4, pourrait être un des contributeurs potentiels de la déstabilisation des plaques en particulier dans l’endotoxémie, elle-même associée aux accidents cardiovasculaires. L’objectif de ce travail a été de définir le rôle du leucotriène B4 dans l’attraction des neutrophiles dans la plaque au cours de l’endotoxémie et de déterminer si les neutrophiles peuvent basculer l’équilibre qui maintient les plaques stables. Nous avons montré que le recrutement des neutrophiles médié par le leucotriène B4 a un impact délétère sur la stabilité des plaques au cours de l’endotoxémie en favorisant l’apoptose et la dégradation de fibres matricielles. En conclusion, cette étude ouvre la voie vers de nouvelles approches thérapeutiques visant à cibler l’axe leucotriène-neutrophiles dans la maladie athérosclérotiqueAtherosclerotic 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
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Yao, Yi. "Sequential Priming of Neutrophils." University of Toledo Health Science Campus / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=mco1389612809.
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Manriquez, 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.
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Neisseria meningitidis est un diplocoque à Gram négatif responsable de méningite et de choc septique. Alors que la méningite est la forme d'infection la plus fréquente, la septicémie fulminante est responsable de 90% de la mortalité imputable à N. meningitidis. La septicémie méningococcique est caractérisée par une éruption purpurique due à des lésions vasculaires. Les observations au niveau histologique révèlent des méningocoques associés aux cellules endothéliales, des thromboses, des hémorragies périvasculaires et des infiltrations de cellules inflammatoires. Les mécanismes conduisant à ces lésions vasculaires ainsi que les raisons pour lesquelles le système immunitaire inné est incapable de contrôler l'infection avant l'atteinte de ce stade pathologique sont inconnus. Dans ce travail de doctorat, nous abordons ces questions en utilisant un modèle murin humanisée par xénogreffe de peau humaine chez des animaux immunodéficients. Nous rapportons que la prolifération bactérienne dans les capillaires est rapide et mène à l'occlusion des vaisseaux en moins de 3 heures post-infection. Dans ce contexte, les macrophages périvasculaires jouent un rôle de sentinelles car ils phagocytent efficacement les bactéries intraluminales adhérentes, aux stades précoces de l'infection et sont essentiels pour recruter les neutrophiles au site d'infection. L'imagerie intravitale et les expériences de déplétion des neutrophiles indiquent que ceux-ci jouent un rôle important dans la destruction des bactéries adhérentes par un processus de migration inverse c'est à dire de l'extérieur vers l'intérieur des vaisseaux et, par conséquent, diminuent les dommages vasculaires induits par les bactéries. L'analyse de la cinétique de recrutement des neutrophiles montre que ceux-ci atteignent un pic de recrutement entre 16h et 24h post-infection chez la souris infectée par voie intravasculaire, comme c'est le cas lors d'une infection naturelle alors que cela ne prend seulement 3h lorsque les bactéries sont injectées par voie intradermique. Ces résultats montrent que la détection intraluminale des bactéries par les macrophages périvasculaires conduit finalement au recrutement des neutrophiles et au contrôle des lésions vasculaires, mais cette réponse dépendante des macrophages périvasculaires est initiée trop tard pour être pleinement efficaceNeisseria 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
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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.
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The disease gonorrhea has plagued mankind at least as long as written records have been kept (Black and Sparling, 1985). N. gonorrhoeae is still an important cause of suffering, infertility, and occasional mortality despite the fact that treatment with antibiotics is relatively easy and highly effective, even with the recent increase in penicillin-resistant isolates (Jephcott, 1986). The continued existence of this public health problem is partly the result of a reservoir of asymptomatic carriers within the community who normally don't seek treatment and continue their usual sexual practices (Handsfield, 1983; Kavli et al., 1984). Asymptomatic carriers do not have the purulent discharge characteristic of gonococcal urethritis and cervicitis in which the neutrophil is such a prominent element. Since IgM is present in only trace amounts on genital mucosa (Schumacher, 1973), and this is the "naturally occurring" antibody against gonococci (Rich and Kasper, 1982); it is not unreasonable to assume that non-opsonic chemotaxis and non-opsonic phagocytosis by PMN may play important roles in initiating the inflammatory response and symptomatology seen with gonorrhea. Further, non-opsonic phagocytic killing may be important in eventually clearing gonococcal infection since the role of specific humoral immunity is limited by the ability of gonococcus to constantly vary its antigenic facade (Zak et al., 1984). I have found that three different gonococcal strains express certain outer membrane proteins of the protein II (P.II) family which stimulate neutrophil phagocytic killing and oxidative metabolism in a highly efficient, dose-dependent manner. Other P.IIs expressed by two of the strains are non-stimulatory. Since all P.IIs have very similar physicochemical properties, these results suggest that a specific receptor-ligand interaction occurs between the gonococcal P.II and some element of the neutrophil plasma membrane. The presence or absence of pili on the gonococcal surface has no apparent effect on the ability of certain P.IIs to stimulate neutrophils. Changes in gonococcal outer membrane protein I and lipopolysaccharide, which are thought to confer serum resistance, also have no apparent effect on P.II stimulation of human PMN. Therefore, gonococcal outer membrane P.II may be an important mediator in the inflammatory response to gonococcal infection. Once gonococci are phagocytized by human PMN killing occurs rapidly and there is no evidence of significant intracellular survival. Non-oxidative killing by human chronic granulomatous disease neutrophils is as effective as the killing seen with normal PMN. Extracellular killing of gonococci does not occur to any appreciable extent.
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GRIMOLIZZI, 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.
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La gravidanza è da considerarsi una condizione pro-inflammatoria dove si osserva un’attivazione dei neutrofili circolanti. Con l'avanzare della gravidanza la concentrazione nel sangue di nucleosomi e mieloperossidasi aumenta e riflette la produzione delle trappole extracellulari dei neutrofili (NETs). Abbiamo dimostrato che in corso di diabete mellito gestazionale (GDM) tale produzione è aumentata in confronto ad una gravidanza fisiologica. Elevati livelli di glucosio e TNF-a, segni tipici presenti in corso di GDM, in vitro agiscono in modo sinergico e sono in grado di pre-attivare i neutrofili ed indurre il rilascio delle NETs. Abbiamo ipotizzato che, lo stato di iperattivazione osservato a livello sistemico possa essere associato ad una aumentata attività leucocitaria a livello placentare. A sostegno della nostra ipotesi, si osserva nei villi coriali isolati da placente GDM un’aumentata infiltrazione di PMNs pro-NETotici in associazione ad un accumulo della neutrofili elastasi (NE). Per valutare un possibile effetto pro-infiammatorio del glucosio a livello placentare, abbiamo incubato cellule di trofoblasto (BeWo) in presenza di un’elevata concentrazione di glucosio e successivamente valutato la produzione di TNF-a. È stato interessante rilevare un aumento nel rilascio di TNF- a tale da indurre un effetto pro-NETotico sui PMN con consequente rilascio della NE. Da recenti ricerche è emerso come in corso di diabete e tumore la NE possa essere internalizzata dalle cellule ed alterare la trasduzione del segnale insulinico attraverso la degradazione del substrato 1 del recettore insulinico (IRS1). Esperimenti in vitro hanno dimostrato che in presenza della NE si osserva una riduzione di IRS1 nelle cellule BeWo ed una diminuzione dell’internalizzazione del glucosio. Poichè l’espressione di IRS1 risulta ridotta nelle placente GDM é verosimile ipotizzare che la massiva presenza di NE ne può essere la causa. In conclusione, i nostri dati suggeriscono che in corso di GDM si verifica un’elevata produzione di NETs ed una massiva infiltrazione di pro-NETotici PMN nella placenta. Queste scoperte dimostrano come la NETosi abbia una significativa utilità diagnostica in corso di GDM e la NE un nuovo potenziale bersaglio terapeutico.Human 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.
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Darbousset, Roxane. "Roles of polymorphonuclear neutrophils in thrombosis." Thesis, Aix-Marseille, 2013. http://www.theses.fr/2013AIXM5071.
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L’hémostase est un processus physiologique permettant de préserver l’intégrité du système vasculaire et de prévenir une perte de sang en réponse à une blessure. En situation pathologique, comme dans le cas de cancers, d’infections ou de maladies cardiovasculaires, il peut y avoir activation de la cascade de coagulation entraînant la formation d’un thrombus.Dans cette étude, nous avons utilisé la microscopie intravitale dans un modèle de blessure au rayon laser pour comprendre les mécanismes cellulaires et moléculaires mis en jeu dans la formation d’un thrombus plaquettaire en conditions physiologiques et pathologiques lors du développement d’un cancer. La première partie de ce travail a consisté à décrire l’implication des polynucléaires neutrophiles dans la formation d’un thrombus. Nous montrons que les neutrophiles sont les premières cellules à s’accumuler au niveau du site de blessure et représentent la principale source de facteur tissulaire menant à la génération de fibrine et à la formation du thrombus. Ces neutrophiles sont nécessaires au recrutement de cellules endothéliales progénitrices (Endothelial colony- forming cells, ECFCs), qui sont des cellules capables de jouer un rôle important dans la réparation vasculaire. Dans une seconde partie, nous avons déterminé, dans des modèles murins adaptés, l’implication de l’activation du FT et des plaquettes dans la thrombose associée au cancer. En conclusion, notre travail donne de nouvelles perspectives dans la compréhension du rôle pathophysiologique des neutrophiles, des cellules progénitrices endothéliales et des plaquettesHemostasis 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
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Haynes, Andrew Paul. "Metabolic abnormalities in uraemic neutrophils." Thesis, University of Nottingham, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305133.
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Cross, Andrew. "Molecular properties of inflammatory neutrophils." Thesis, University of Liverpool, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250467.
Full textBooks on the topic "Neutrophils"
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S, Abramson Jon, and Wheeler J. Gary, eds. The Neutrophil. Oxford: IRL Press at Oxford University Press, 1993.
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Voisin, Cyr, N. Wierzbicki, and J. P. Revillard. Mucosal immunity: IgA and polymorphonuclear neutrophils. Suresnes Cedex (France): Fondation Franco-Allemande, 1985.
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Tuominen-Gustafsson, Helena Birgitta. Calcium signalling pathways in human neutrophils. Åbo: Åbo Akademis Förlag, 1998.
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Alonso-Fernández, Patricia. Neutrophils in biological age and longevity. New York: Nova Science Publishers, Inc., 2011.
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Leino, Lasse. Studies on the function and expression of Fc-gamma and complement receptors on human neutrophils. Turku: Turun Yliopisto, 1991.
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1952-, Hallett Maurice B., ed. The Neutrophil: Cellular biochemistry and physiology. Boca Raton, Fla: CRC Press, 1989.
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Hallett, Maurice B. The molecular and ionic signalling of neutrophils. New York: Chapman & Hall, 1997.
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I, Gabrilovich Dmitry, ed. The neutrophils: New outlook for old cells. 2nd ed. Hackensack, N.J: Imperial College Press, 2004.
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Brumell, John H. Phosphorylation-dependent signalling mechanisms in human neutrophils. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.
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Hallett, Maurice B. The molecular and ionic signaling of neutrophils. Austin. Tex: Landes Bioscience, 1997.
Find full textBook chapters on the topic "Neutrophils"
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Whyte, Moira. "Neutrophils." In Cellular Mechanisms in Airways Inflammation, 125–46. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8476-1_4.
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Zurier, Robert B. "Neutrophils." In 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.
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Cuzzocrea, Salvatore. "Neutrophils." In 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.
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Jain, Rohit, Andrew J. Mitchell, Szun S. Tay, Ben Roediger, and Wolfgang Weninger. "Neutrophils." In Immunology of the Skin, 147–67. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55855-2_9.
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Clausen, Torben, José Luis Trejo, Mark P. Mattson, Alexis M. Stranahan, Joanna Erion, Rosa Maria Bruno, Stefano Taddei, and Melinda M. Manore. "Neutrophils." In 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.
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Gevaert, Elien. "Neutrophils." In Chronic Rhinosinusitis, 69–79. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-0784-4_9.
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Zweiman, Burton. "Neutrophils." In Inflammatory Mechanisms in Allergic Diseases, 77–95. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/9780429134432-6.
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Kuijpers, Taco W., Timo K. van den Berg, and Dirk Roos. "Neutrophils Forever …" In Phagocyte-Pathogen Interactions, 1–26. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816650.ch1.
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Oliveira, André Gustavo, Rodrigo Guabiraba, Mauro Martins Teixeira, and Gustavo Batista Menezes. "Tumor-Associated Neutrophils." In 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.
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Leino, Lasse. "Chemotaxis of Neutrophils." In Encyclopedia of Immunotoxicology, 176–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_251.
Full textConference papers on the topic "Neutrophils"
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Selak, M. A., M. Chignard, and J. B. Smith. "CHARACTERIZATION OF A NEUTROPHIL CPYMOTRYPSIN-LIKE ENZYME THAT ACTIVATES PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643157.
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Communication between neutrophils and platelets was previously investigated by measuring platelet aggregation, serotonin release and changes in cytosolic free calcium subsequent to specific stimulation of neutrophils by fMet-Leu-Phe (FMLP) in a suspension of both cell types. The addition of the chemotactic peptide was shown to elicit secondary platelet activation as a consequence of primary stimulation of neutrophils. Cell-free supernatants from FMLP-stimulated neutrophils were capable of inducing platelet activation thus demonstrating that a factor released bv neutrophils was responsible for the observed platelet responses. After eliminating classical platelet agonists as the acitive agent, it was shown that an enzyme termed neutroohilin induced platelet calcium mobilization, secretion and aggregation. The current studies were conducted to characterize the mediator released bv neutrophils. Neutrophilin bound bo cation exchange resins but failed to bind to anion exchangers. The biological activity associated with neutroohilin was unaffected by leupeptin, only very weakly diminished by N-bosyl-Lvs-chloromethvl ketone and was strongly inhibited by N-tosvl-Phe-chloromethvl ketone, aloha-l-antitrvpsin, soybean trypsin inhibitor and Z-Glv-Leu-Phe-chloromethvl ketone. Neutroohilin was released from stimulated neutrophils only after cytochalasin B treatment, as was beta-glucuronidase, suggesting that both enzymes are located in azurophilic granules. Neutroohilin-induced platelet activation was inhibited bv antiserum to human catheosin G in a dose-deoendent manner but was unaffected by antiserum to human elastase or alpha-fetoprotein. The inhibitor sensitivity, immunological cross-reactivity, ionic properties and probable subcellular localization indicate that neutrophilin is a cationic chymotrvosin-like enzyme related, if not identical to, catheosin G. Neutroohilin-induced platelet activation could explain different pathological events in which platelets and neutroohils are known to be involved.
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Teo, Soo Kng, Kim H. Parker, and K. H. Chiam. "Viscoelastic Finite-Element Modelling of Neutrophil Deformation in a Tapered Micropipette." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-191099.
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In this paper, we discuss the results arising from using a viscoelastic, axisymmetric finite-element model [1] to study the aspiration of neutrophils into a tapered micropipette [2]. The key feature of our model is that we take into account the experimentally observed temporal variations in the rheological properties of deforming neutrophils [3]. We show that our model successfully reproduces the equilibrium state reached by a neutrophil subjected to a constant step pressure [2]. We are also able to extract quantitative information about the rate at which the rheological properties of the neutrophil change. Such information may be difficult to obtain directly from the experiments themselves. Thus, our approach illustrates the usefulness of computational modeling as a complement to experiments.
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Sounbuli, K., N. L. Mironova, O. V. Markov, and L. A. Alekseeva. "A COMPARATIVE STUDY OF DIFFERENT ISOLATION PROTOCOLS OF MURINE NEUTROPHILS FROM BONE MARROW AND SPLEEN." In OpenBio-2023. ИПЦ НГУ, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-52.
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Neutrophils are considered the main player in innate immunity. In the last few years, they were involved in different physiological conditions and diseases. However, progress in the field of neutrophil biology is relatively slow due to several difficulties in neutrophil isolation and studying in culture. Here we compare three protocols based on density-gradient method and immunomagnetic method for mouse neutrophil isolation from the bone marrow and spleen.v
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Marcus, A. J., L. B. Safier, H. L. Ullman, N. Islam, M. J. Broekman, and C. V. Schacky. "NEW EICOSANOIDS FORMED DURING PLATELET-NEUTROPHIL INTERACTIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644626.
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In physiologic and pathologic processes such as hemostasis, thrombosis and inflammation, multiple cell types are brought into close proximity - thereby increasing the possibility of metabolic interactions in the microenvironment. Activated platelets synthesize12-hydroxyeicosatetraenoic acid (12-HETE) in the presence or absence of aspirin. During a cell-cell interaction, platelet 12-HETE is metabolized by a cytochrome P-450 enzyme system in unstimulated neutrophils to 12.20-dihydroxyeicosatetraenoic acid (12,20-DiHETE). Recently, we observed time-dependent formation of a new eicosanoid following exposure of neutrophils to 12-HETE. This compound is more polar than the parent eicosanoid 12,20-DiHETE (reversed-phase HPLC). Incubation of purified 12,20-DiHETE with neutrophils resulted in a progressive decrease in the 12,20-DiHETE with increasing formation of the polar metabolite. In the absence of neutrophils, 12.20-DiHETE was quantitatively unchanged. The new metabolite of 12.20-DiHETE has been tentatively identified as 12-hydroxyeicosatetraen-l,20-dioic acid. The UV absorption maximum of the new compound is 237 nm which is identical to that of 12-HETE and 12,20-DiHETE. 20-hydroxy-LTB4 is the omega-hydroxylated derivative of the pro-inflammatory eicosanoid LTB4. When added to neutrophils 15 sec prior to 12,20-DiHETE, equimolar concentrations of 20-hydroxy-LTB4 (2.8uM) inhibited formation of the new metabolite by 28%. A concentration of 8uM 20-hydroxy-LTB4 inhibited the reaction by 49%. These results indicate that the neutrophil enzyme system responsible for conversion of 20-hydroxy-LTB4 to 20-carboxy-LTB4 may also be involved in further metabolism of-12,20-DiHETE. Neutrophil homogenization resulted in loss of the capacity to transform 12.20-DiHETE to the new metabolite despite pretreatment with DFP and addition of NADPH. Our data provide further evidence for the occurrence of transcellular metabolic events during thrombosis and the inflammatory response.
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Coeffier, E., D. Joseph, and B. B. Vargaftio. "PLATELET-LEUKOCYTE INTERACTION: ACTIVATION OF RABBIT PLATELETS BY FMLP-STIMULATED NEUTROPHILS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643158.
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The interaction of neutrophils and platelets may be important in inflammation. We have studied the effect of the chemotactic peptide, N-formyl-methionyl-leucy1-phenylalanine (FMLP) on cells in whole rabbit blood or in mixture of purified rabbit platelets and neutrophils. In whole blood, FMLP triggered an aggregation (measured by electrical impedance) dependent upon the concentration of FMLP (9.9± 0.7 and 5.2+1.2 ohms at 1 and 0.01 uM FMLP resp.). This aggregation was accompanied by a strong decrease in platelets counts (54.6± 6.0 and 45.6± 3.8% for 1 and 0.01 uM FMLP resp.) and by a smaller decrease in neutrophils counts (25.0± 1.9 and 12.9± 1.7% at 1 and 0.01 uM FMLP resp.). When platelets were incubated in the presence of neutrophils, the addition of 0.1 uM FMLP induced a marked aggregation (50.0± 1.6 versus 19.5± 1.6% of light transmission,n=8,p< .001), ATP secretion (8.4± 1.0 versus 0.1± 0.1 nmol/ml,n=6,p< .001) and a marked decrease of platelets counts. FMLP induced aggregation of purified neutrophils and release of lysozyme but lacked direct platelet-stimulating effect. The release of lactate dehydrogenase and lysozyme were unchanged under the interaction conditions. Our results indicate that the stimulation of neutrophils by FMLP induces platelet activation both in whole blood and on isolated cells. The platelet activation was reduced by about 30% with lOOuM aspirin or indomethacin and by about 70% with lOOuM BW 755C. The two PAF-acether antagonists, BN 52021 (lOOuM) and WEB 2086 (luM) suppressed platelet activation by 70-80%. Neutrophil supernatant induced platelet activation only when neutrophils were stimulated by FMLP in the presence of bovine serum albumin (BSA,0.25%). Rabbit neutrophils stimulated in the presence of BSA by 1 uM FMLP formed 2 nM PAF-acether of which only 50% were released to the extra-cellular medium. WEB 2086 (luM) inhibited totally the formation and the release of PAF-acether. These data indicate that both arachidonic acid-metabolites and PAF-acether participate in platelet activation by FMLP-activated neutrophils.
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Bell, D., M. Jackson, C. MacRae, A. L. Muir, and J. Dawes. "NEUTROPHIL ELASTASE IS A MARKER OF NEUTROPHIL ACTIVATION IN ACUTE MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643020.
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Elastase is released from human neutrophils as a result of active secretion, phagocytosis or cell lysis. It is a broad-spectrum protease which not only hydrolyses the major components of tissue matrix, but can also affect platelet aggregation, coagulation and fibrinolysis. Neutrophils localise at the site of myocardial infarction and have been implicated in subsequent cell damage. A radioimmunoassay was developed which detects elastase complexed to its inhibitors α2- antitrypsin and α2-macroglobulin as wen as the free enzyme. Plasma concentrations of elastase in 31 healthy controls were 21.3 ± 13.8 ng/ml, and did not differ significantly from those in 22 patients with stable angina (23.6 ± 8.6 ng/nl). In 19 patients with myocardial infarction, however, plasma elastase levels rose to a peak within 48 hours of infarct which was significantly higher than normal levels (95.1 < 83.7; P < 0.001), and then declined. Correction of the data for neutrophil count did not affect the significance of the observed differences. Measurement of whole blood elastase reflected the neutrophil count and was not otherwise informative. Thus, neutrophils are activated after myocardial infarction and release sufficient elastase for it to be detected systemically. This may extend tissue damage and affect coagulation and fibrinolysis at the site of infarction.
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Muylle, L., C. Van Brussel, D. R. van Bockstaele, and M. E. Peetermans. "IN VITRO NEUTROPHIL ACTIVATION BY PLASMA OF STORED PLATELET CONCENTRATES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644686.
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A previous study showed an effect of storage time of platelet concentrates (PLC) on the frequency and severity of reactions to platelet transfusion.As most of the leukocytes were removed from the PLC prior to transfusion, it was suggested that at least part of the reactions were caused by the transfusion of cell products, accumulated during conservation of the PLC.This idea is supported by the finding of high histamine levels in PLC after 5 days storage.In order to test for the presence of substances causing neutrophil activation, samples from 7 PLC were taken at various storage times and incubated for 30 minutes at 37°C with neutrophilic granulocytes obtained from healthy donors. Binding of a monoclonal antibody specific for a neutrophil-associated membrane glycoprotein (gp 170) was analyzed by indirect immunofluorescence. (CLB 13.9,kindly given by P. Tetteroo).It is known that the expression of gp 170 is enhanced by stimulation of the neutrophil.Fluorescence intensity was quantified by flow cytometry (Ortho cytofluorograf 50-H).Results were expressed as an activation ratio (AR) (ratio of the median fluorescence intensity over that of negative control neutrophils).At day 0 no activation was recorded (AR = 1±0.09,n = 7). In contrast, the supernatant plasma of PLC stored for 7 days caused an elevated AR in 4/7 PLC (AR = 3.20±1.20, n = 4).For comparison the AR of the positive control was 3.66±0.63 (n = 5).In 2 PLC activation was already observed after 1 day storage.The increased expression of gp 170 was not correlated with the histamine level, the lactate dehydrogenase level, the leucocyte or platelet count in the PLC.These preliminary results indicate the presence of factors causing in vitro activation of neutrophils in the supernatant plasma of some stored PLC.Further investigations are needed to confirm these results, to identify the responsible factor(s) and to study the clinical relevance of this finding.
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Farache Trajano, Luiza, Rebecca Moore, and Quentin Sattentau. "The Presence of Chemical Cross-Linking Stabilises HIV-1 Envelope Glycoprotein Trimer Antigens in a Model of Intramuscular Immunisation." In Building Bridges in Medical Science 2021. Cambridge Medicine Journal, 2021. http://dx.doi.org/10.7244/cmj.2021.03.001.4.
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Background: The HIV-1 envelope glycoprotein (Env) is the target of antigen design for antibody- based vaccination. In 2019, four trimeric Env vaccines entered an experimental trial: ConM, ConS, and their cross-linked counterparts. The trimers were formulated with MPLA adjuvant. Studies have demonstrated that adjuvants trigger neutrophil infiltration. Neutrophils activate and degranulate releasing proteases, namely elastase and cathepsinG. Aims: To assess the stability and immunogenicity of these vaccines in the presence of adjuvant- recruited neutrophils and their proteolytic enzymes. Methods: Trimers were incubated with commercially-sourced proteases. To analyse stability, samples were reduced, denatured and separated using gel electrophoresis. To assess antibody binding, a trimer-protease incubation was followed by an ELISA. To establish more physiologically relevant conditions, harvested neutrophils were exposed to various adjuvants. The supernatant, shown to contain elastase, was incubated alongside the vaccines. The reducing and denaturing gels, as well as the ELISA, was repeated. Results: Gel analysis revealed that un-crosslinked trimers underwent significant digestion whereas cross-linking conferred enhanced stability. In the presence of neutrophil-sourced protease-containing-supernatant, trimers displayed resistance to digestion. The differential stability profile of Env trimers when exposed to commercially sourced compared to supernatant- derived proteases may be due to the inhibitory effect of human serum on elastase. Antibody epitopes were maintained in vitro. Conclusion: The vaccine antigens are sensitive to enzymatic degradation. This is reduced by cross-linking and human serum.
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Alteraifi, Abdullatif M., and Doncho V. Zhelev. "Cytoskeleton Rearrangement in Activated Human Neutrophils." In ASME 1996 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1996. http://dx.doi.org/10.1115/imece1996-1110.
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Abstract The crawling of the neutrophil is essential for its physiological and pathological activity. The neutrophil crawls by projecting pseudopods in the direction of a higher chemoattractant concentration in a process known as chemotaxis. In this process, the cell initially adheres tightly to the present substrate and then rearranges its cytoskeleton. Finally, the ceil body contracts, which results in cell movement. The rearrangement of the cytoskeleton is believed to be a crucial component of cell motility (Cunningham et al., 1992) which determines the overall rate of crawling (Zigmond, 1993). Therefore, it is important to find means of characterizing this in different conditions in order to reveal the role of the different factors in neutrophil motility. The available assays for studying neutrophil motility has one common disadvantage namely, they all produce large contact areas between the cell and the supporting substrate. This large contact area can be coupled with adhesion, which may alter neutrophil activation. To avoid the creation of large contact area with the cell surface in our experiments, we used micropipets. The use of micropipets allow both to minimize the contact area and to manipulate the cellular environment. Using this technique we can produce single pseudopods on individual cells by delivering a known concentration of a chemoattractant to the cell surface. We use the chemoattractant N-formyl-methionyl-leucyl-phenylalanine (fMLP) and by employing the above technique we were able to produce highly oriented cylindrical pseudopods on initially passive neutrophils (Fig. 1). Also, by using another micropipet assay (Zhelev and Hochmuth, 1995) we produced pseudopod-like structures in chemoattractant free solution, by pulling a tether from the cell surface (Fig. 2). In both cases we observe the formation of a dense F-actin network next to the leading edge of the pseudopod or pseudopod-like structure. Also, when the pseudopod or the pseudopod-like structure extends away from the cell body we observe the cell granules penetrating the network region. This penetration shows that there are vacancies in the network region, which indicate network depolymerization. The depolymerization of the network provides conditions for actin turnover (Theriot and Mithchison, 1991).
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Shirai, A., and T. Hayase. "Effect of Retention Time of Neutrophils in Alveolar Capillaries on Increase in Their Concentration in the Capillary Network." In ASME/JSME 2007 5th Joint Fluids Engineering Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/fedsm2007-37653.
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It is said that neutrophils, a kind of leukocytes, can be retained in pulmonary alveolar capillary bed, even in normal lungs, resulting in higher concentration than in systemic circulation due to their relatively low deformability, and the concentrated neutrophils help the lung to effectively eliminate the enemies invading from outer air. The authors have developed a model to simulate the flow of neutrophils through an alveolar capillary network, considering the cells’ low deformability as the dominant factor for the retention. Flow of a suspension of neutrophils in plasma through a simplified lattice alveolar capillary network model was numerically simulated to investigate the effect of the retention on the increase in the concentration ratio of the cells between in the network and in the suspension. The numerical result showed that the ratio was lower than the experimentally obtained value. Other possible factors to influence the cell’s retention time are friction and adhesion of the cell on the endothelium. In the last study, effect of the retention time of the cells in individual capillary segments on the increase in the concentration ratio was investigated to suggest the ratio may have an upper limit no matter how long the retention time is extended. In this paper, the authors investigated the contribution of various parameters which affect transit time of a neutrophil through a single capillary segment to the relationships between the retention time and the concentration ratio. Finally, it was shown that the number of cells in the network increased to approach a finite value as the increase in the coefficient, independent of the cell property, concentration of the cells in the suspension or the capillary shape. Transition of the relationship was changed with the parameters.
Reports on the topic "Neutrophils"
1
Boston, Mark E. Effects of Nasal Saline Spray on Human Neutrophils. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada406691.
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Viksna, Ludmila, Oksana Kolesova, Aleksandrs Kolesovs, Ieva Vanaga, and Seda Arutjunana. Clinical characteristics of COVID-19 patients (Latvia, Spring 2020). Rīga Stradiņš University, December 2020. http://dx.doi.org/10.25143/fk2/hnmlhh.
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Data include following variables: Demographics, epidemiological history, comorbidities, diagnosis, complications, and symptoms on admission to the hospital. Also, body’s temperature and SpO2. Blood cells: white cells count (WBC), neutrophils (Neu), lymphocytes (Ly), eosinophils (Eo) and monocytes (Mo), percentages of segmented and banded neutrophils, erythrocytes (RBC), platelet count (PLT), hemoglobin (Hb), and hematocrit (HCT); Inflammatory indicators: erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP); Tissue damage indicators: alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and troponin T (TnT); Electrolytes: potassium and sodium concentration; Renal function indicators: creatinine and glomerular filtration rate (GFR); Coagulation tests: D-dimer, prothrombin time, and prothrombin index on admission to the hospital.
3
Liang, Feixin. Progress in Liquid Biopsy: A possible role of neutrophils. Science Repository, August 2018. http://dx.doi.org/10.31487/j.cor.2018.02.004.
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Boston, Mark E., G. C. Frech, Enrique Chacon-Cruz, E. S. Buescher, and David G. Oelberg. Surfactant Releases Internal Calcium Stores in Neutrophils by G Protein-Mediated Pathway. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada413640.
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Haight, Gary. Inquiry into the causes and significance of cytoplasmic vacuolation of neutrophils in the peripheral circulation. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.5283.
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Youngman, Sara. The Chemotactic Response of Neutrophils to Components of the Sera of Mice Infected with Trichinella spiralis. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.6942.
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Bowles, Charles A., and Andrew Baum. Investigation of Stress Induced Alterations in Neutrophil Function. Fort Belvoir, VA: Defense Technical Information Center, May 1991. http://dx.doi.org/10.21236/ada237002.
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Trofimenko, A., M. Mamus, S. Bedina, E. Mozgovaya, and 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.
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Bechev, Blagovest, Moni Magrisso, Stilian Stoeff, and 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, March 2019. http://dx.doi.org/10.7546/crabs.2019.03.15.
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Goldman, Gideon, Richard Welbourn, C. R. aleri, David Shepro, and Herbert B. Hechtman. Leukotriene B4 and Thromboxane A2 are Essential Cofactors in CD 18 Dependent Neutrophil Diapedesis. Fort Belvoir, VA: Defense Technical Information Center, July 1990. http://dx.doi.org/10.21236/ada360180.
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