Relevant bibliographies by topics / Immunology, Neutrophil

Academic literature on the topic 'Immunology, Neutrophil'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Immunology, Neutrophil"

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Cavallaro, Elena C., Kar-Kate Liang, Kevin D. Forsyth, and Dani-Louise Dixon. "Neutrophil polarization in the airways of infants with bronchiolitis." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 55.30. http://dx.doi.org/10.4049/jimmunol.198.supp.55.30.

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Abstract Pulmonary neutrophilia is observed in pediatric patients with viral-induced bronchiolitis. Despite an alleviation in clinical symptoms, our findings suggest that airway neutrophil infiltration and activation does not appear to resolve by discharge in hospitalized infants. The recent identification of neutrophil plasticity and polarization into distinct phenotypic pro-inflammatory (N1) and immunosuppressive (N2) subsets provides an unexplored avenue for regulation of the neutrophilic inflammatory response in bronchiolitis. Admission nasopharyngeal aspirate (NPA) samples were assessed from twelve bronchiolitic infants presenting to Flinders Medical Centre, Adelaide, Australia in 2013. An overall strong positive correlation between N2 soluble mediator TGF-β1 and the percentage of neutrophils stained for N2 marker MMP-9 was observed; with no correlation observed between TGF-β1 and neutrophils positive for N1 marker ICAM-1. In 2015 and 2016, eleven bronchiolitic infants provided consecutive NPAs across hospitalization. In both cohorts, concentrations of active TGF-β1 detected were comparable to levels previously identified to significantly suppress neutrophil activity in vitro (>1 pg/mL). Temporal assessment of neutrophil polarization is underway. The detection of pre-established neutrophil polarizing mediators, and the correlation of these mediators with different neutrophilic subsets within NPAs indicates a potential N1/N2 paradigm occurring within the airways of bronchiolitic infants. Further investigation is merited, with analyses over disease trajectory and by disease severity required to assess biological significance.
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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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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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Harvath, L., K. B. Yancey, and S. I. Katz. "Selective inhibition of human neutrophil chemotaxis to N-formyl-methionyl-leucyl-phenylalanine by sulfones." Journal of Immunology 137, no. 4 (August 15, 1986): 1305–11. http://dx.doi.org/10.4049/jimmunol.137.4.1305.

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Abstract The therapeutic efficacy of the sulfones, dapsone, and sulfoxone in neutrophilic dermatoses may be related to the effects of these drugs on neutrophil function. Therefore we determined whether neutrophil chemotactic migration to various chemoattractants could be inhibited by sulfones in vitro. The chemotactic responses of human neutrophils from healthy donors were tested by using N-formyl-methionyl-leucyl-phenylalanine (F-met-leu-phe), purified human C5a, and leukocyte-derived chemotactic factor (LDCF). Therapeutic concentrations of sulfones selectively inhibited neutrophil chemotaxis to F-met-leu-phe, but did not affect neutrophil chemotaxis to LDCF or C5a. Inhibition of neutrophil chemotaxis to F-met-leu-phe was induced by both dapsone and sulfoxone at a concentration of 10 micrograms/ml without affecting random migration, and the inhibition was reversed by washing the neutrophils. When dapsone- and sulfoxone-treated neutrophils (100 micrograms/ml) were stimulated with F-met-leu-phe, neutrophil superoxide generation was not inhibited. Sulfapyridine (10 micrograms/ml) also selectively inhibited neutrophil chemotaxis to F-met-leu-phe; however, sulfamethoxazole and sulfisoxazole did not affect chemotaxis. The inhibitory effects of dapsone, sulfoxone, and sulfapyridine could not be demonstrated with granulocytes from rabbits or guinea pigs nor with human monocytes. Experiments with radiolabeled dapsone showed rapid, nonspecific, and reversible binding of dapsone to human neutrophils. These data suggest that a mechanism of action of sulfones in neutrophilic dermatoses may be a selective inhibition of neutrophil migration to as yet undefined chemoattractants in the skin.
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Wang, Jun-Xia, and Peter Nigrovic. "CD177 participates in a novel mechanism for regulating neutrophil recruitment (P3093)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 43.9. http://dx.doi.org/10.4049/jimmunol.190.supp.43.9.

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Abstract Background: Neutrophils are the sine qua non of inflammatory arthritis, and contribute to pain, swelling, and tissue injury, rendering neutrophil migration to the joint a potential therapeutic target. We recently found that the murine neutrophil surface protein Ly6G modulates chemotaxis via interaction with β2 integrins. Whereas CD177 is a neutrophil-specific human protein in the same gene family, we sought to identify the role of CD177 in human neutrophil recruitment. Method: Flow cytometry was used to analyze the levels of cell surface proteins in circulating neutrophils and in neutrophils from inflamed joints. Fluorescence lifetime imaging microscopy/Fluorescence resonance energy transfer assay (FLIM/FRET) was used to quantify CD177-β2 integrin interactions. Result: In patients with rheumatoid arthritis, synovial neutrophils exhibit higher levels of surface CD177 expression comparing with blood neutrophils. Using FLIM/FRET, ~40% CD11a and ~20% CD11b β2 integrins interact with CD177 on surface of resting blood neutrophils. In vitro, a specific CD177 antibody inhibits LTB4-induced conformational activation of CD11b β2 integrin, which is correlated with an impaired neutrophil migration towards LTB4 in anti-CD177 treated cells in a transwell system. Conclusion: CD177 regulates neutrophil chemotaxis and may serve as a potential neutrophil-specific therapeutic target in neutrophilic inflammatory diseases such as arthritis.
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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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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.
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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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Brinkworth, Jessica F., Kathrine Van Etten, Priya Bhatt, Keaton McClure, Negin Valizadegan, Minkyu Woo, Suvanthee Gunasekera, Yaravi Suarez, and Brian Aldridge. "Functional comparison of human and non-human primate neutrophil responses." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 73.21. http://dx.doi.org/10.4049/jimmunol.202.supp.73.21.

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Abstract Humans and apes are neutrophilic, maintaining high levels (50–70% of circulating leukocytes) of this short-lived, highly reactive cell type (neutrophils), while most primates maintain significantly lower proportions(20–40% circulating leukocytes). Neutrophils are key limiters of bacterial and parasitic infection, amplifying inflammation, phagocytosing and presenting, and trapping invading foreign material, as well as committing bystander tissue damage in these efforts. The comparative neutrophilia of humans, therefore, suggests alterations in neutrophil activities such that higher proportions are both required and tolerated in this species. To address this possibility, we analyzed transcriptomic, and cell physiological responses of neutrophils from humans, and two biomedically important primates, rhesus macaque and common marmoset. Cells were isolated via a density gradient and stimulated with 1ng-1ug of lipopolysaccarhide (LPS) from Escherichia coli K12 or the bacteria itself (MOI 10:1) for 1–3 hours. Transcriptomic responses were captured by RNAseq, and physiological responses [phagocytosis, apoptosis, extracellular trapping (NETing)] by fluorescent microscopy. The species differed strongly the expression of genes in innate immune and cell trafficking pathways. Overall, primates exhibited NETing and apoptosis sensitivity to even the lowest dose of LPS. Humans, however, displayed a unique complement of neutrophil antimicrobial responses - phagocytosing and apoptosising more, while NETing less than the other species. These results suggest inter-species differences in important neutrophil antimicrobial strategies that may impact interpretation of primate biomedical models.
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Shelite, Thomas R., Nicole L. Mendell, Donald H. Bouyer, David Hughes Walker, and Lynn Soong. "The role of neutrophils during Orientia infection." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 66.28. http://dx.doi.org/10.4049/jimmunol.196.supp.66.28.

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Abstract Scrub typhus is a seriously neglected disease with approximately one-third of the world’s population at risk of being infected with Orientia tsutsugamushi, and the occurrence of over one million scrub typhus cases annually illustrate its importance in global health. All scrub typhus case studies that report blood cell counts, describe neutrophilia during the course of infection. Patients with confirmed scrub typhus have significant increases in activated neutrophil proteins in serum, and the increase of neutrophil recruiting cytokines. We also observed neutrophilia as well as neutrophil recruitment to infected tissues in intravenously infected mice, suggesting key role for neutrophils in scrub typhus disease progression. To determine the role of neutrophils in this infection, female C57BL/6 mice were lethally challenged, and neutrophils were depleted one day prior to infection (D−1) or six (D+6) days post infection. The effects of neutrophil depletion were observed to be dependent on the time post infection. Animals depleted early (D-1) exhibited more severe pathology at an earlier time point and had disease progression similar to non-depleted animals but had greater survival. Animals depleted 6 dpi recovered weight, and signs of illness had resolved by 12 dpi. Histopathology demonstrated decreased cellular infiltrates when compared to infected, non-depleted animals. Depletion of neutrophils decreased mortality independent of when depleted, but only depletion 6 dpi resulted in amelioration of signs. These data suggest an important role of neutrophils in tissue pathology and disease progression during scrub typhus infection.
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Dissertations / Theses on the topic "Immunology, Neutrophil"

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Eckert, Rachael. "Molecular Mechanisms of Neutrophil Migration." NCSU, 2007. http://www.lib.ncsu.edu/theses/available/etd-10312007-134315/.

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This work is an investigative look behind the mechanisms of neutrophil migration. Each of three chapters involves exploration into a different signaling pathway important for migration downstream of chemoattractant stimulation through inhibition of a kinase or disruption of the function of an effector and examination of the effects on migration, adhesion, and actin reorganization in primary human or equine neutrophils. Chapter II examines the requirement for the signaling molecule p38 Mitogen Activated Kinase (MAPK) in equine neutrophil chemotaxis through use of the p38 specific inhibitor SB203580. SB203580 reduced LTB4- and PAF-induced migration and disrupted the ability of cells to polarize, but did not affect b2 integrin-dependent adhesion or surface b2 integrin expression. Chapter III is a comprehensive inquiry into the regulation of the phosphorylation of serine 157 of the cytoskeletal protein Vasodilator-stimulated Phosphoprotein (VASP). The rapid and transient phosphorylation of VASP serine 157 corresponded with F-actin levels in chemoattractant-stimulated human neutrophils. fMLF-induced serine 157 phosphorylation was abolished by pretreatment with the PKA inhibitor H89 and the adenylyl cyclase inhibitor SQ22536. In contrast, fMLF-induced serine 157 phosphorylation was unaffected by PKC inhibitors, PKG inhibitors, and the CamKII inhibitor KN-62. Inhibition of adhesion did not alter fMLF-induced VASP phosphorylation or dephosphorylation. This study demonstrated that chemoattractant stimulation of human neutrophils induces a rapid and transient PKA-dependent and adhesion-independent VASP serine 157 phosphorylation. Chapter IV probed into the function of the actin binding protein and PKC substrate Myristoylated Alanine-Rich C-kinase Substrate (MARCKS) through utilization of a cell permeant peptide derived from the MARCKS myristoylated aminoterminus (MANS peptide). Treatment of isolated human neutrophils with 50 μM MANS, but not a scrambled control peptide, significantly inhibited their migration and adhesion in response to fMLF, IL8, or LTB4. MANS significantly reduced F-actin content in neutrophils 30s after fMLF-induced polymerization, but did not alter the ability of cells to polarize, spread, or upregulate surface b2 integrin expression. These data provided evidence that MARCKS, via its myristoylated aminoterminus, is a key regulator of neutrophil migration and adhesion.
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Rochon, Yvan P. (Yvan Pierre). "Dynamics of neutrophil aggregation." Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=70210.

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Neutrophil aggregation has been widely evaluated from changes in light transmission. Using direct particle counting, we demonstrated that light transmission does not accurately reflect aggregation, and showed that in contrast to previous reports, newborn neutrophils do not aggregate irreversibly. We developed a flow cytometric technique to measure the kinetics of neutrophil aggregation, including latent times for onset of aggregation, initial forward and reversal rates, and maximal extents of aggregation. The kinetics of neutrophil aggregation were related to changes in initial cell concentration, stir speed (shear), and activator type and concentration. Physiologic activators stimulated reversible aggregation, accompanied by an exponential decay in aggregatory potential with increasing time. The fraction of occupied activator receptors was found to correspond to the fraction of maximal rates or extent of aggregation. Monoclonal antibodies were used to show that neutrophil aggregation is mediated by the Mac-1 integrin (CD11b/CD18). Direct measurements of aggregation have enhanced our understanding of the (patho)physiologic process of neutrophil aggregation.
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Macdonald, Elizabeth A. "Bovine neutrophil functionality in mastitis resistance." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=68211.

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Diapedesis, phagocytosis and microbicidal activity are important parameters of neutrophil functionality and thus outcome of mastitis. An in vitro model of an "alveolar pavement" using the MAC-T3 bovine mammary epithelial cell line was developed to assess neutrophil diapedesis. Features of this biologically-meaningful barrier include: characteristic transepithelial resistance, tight junction complexes and polarity. Continuous transepithelial resistance measurements showed no significant changes throughout the assay period. Neither a Staphylococcus aureus challenge ($1 times10 sp7$ and $2 times10 sp9$ cfu/ml), or the presence of neutrophils, both resting and challenged had any deleterious effects on monolayer integrity over a short term (1-2 h) exposure. Neutrophils, both resting and challenged gave no indication of causing damage to the epithelium over the short term. Neutrophils isolated from proven sires and evaluated for phagocytic activity were found to differ significantly (p $<$ 0.05) in activity, rate and capacity to uptake particles. Correlations between phagocytic parameters and production traits were negative and small in magnitude. Microbicidal activity of neutrophils isolated from proven sires showed a highly significant variation between animals due to test day (p $<$ 0.001), however variation due to source of cells (i.e. animal) was not significant. in vitro analysis of diapedesis and phagocytosis is promising as a tool for the assessment of resistance or susceptibility to mastitis.
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Bradford, Elaine Alison. "Proposed in vitro model of neutrophil swarming in a chronic, low-level inflammatory state." Thesis, Virginia Tech, 2019. http://hdl.handle.net/10919/102737.

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Chronic, low-grade inflammation is an underlying condition across a globally increasing number of debilitating diseases. These diseases include obesity, atherosclerosis, and diabetes and their resultant low-grade inflammation can be effectivity modeled with low dose stimulants such as lipopolysaccharide (LPS). While the innate immunity plays a significant role in fighting infectious disease, an initial exposure to low dose LPS hinders secondary infection clearance and pre-disposes murine models for fatal sepsis. Neutrophils are the most prevalent circulating innate immune cell and their homotypic aggregation, or swarming, is a key mechanism in clearing pathogens greater than 20 μm in size. We hypothesize that neutrophil swarming ability is altered when in a low dose LPS primed state; potentially leading to an overall altered innate immune response in the face of infection. However, an in vitro model does not currently exist to reliably quantify and compare neutrophil swarms across treatment groups. Here we propose a novel model utilizing fungal zymosan coated beads as a uniform target to which neutrophils may swarm.
Master of Science
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Kirsch, Richard. "Characterisation of fibrinogen and fibrin proteolysis by the neutrophil membrane." Doctoral thesis, University of Cape Town, 1999. http://hdl.handle.net/11427/26928.

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Recent studies have identified a novel 600 kDa neutrophil membrane associated protease which degrades fibrinogen, fibrin and C-reactive protein (CRP) during incubation of these ligands with phorbol 12-myristate 13-acetate (PMA, 5-10 ng/ml) stimulated neutrophils. This proteolysis is predominantly an extracellular event which occurs through a ligand dependent release of this protease from the neutrophil. Degradation products arising from this proteolysis not only become neutrophil associated but influence a number of important processes occurring in inflammation and coagulation. The aim of the present 'study was to purify and further characterize this protease and investigate the location of the neutrophil associated fibrinogen and fibrin degradation products. Whilst enzyme purification procedures were unsuccessful, several observations made during these attempts suggested that the neutrophil membrane associated proteolytic activity displayed similar characteristics to proteases of the azurophil granule. The proteolytic activity of the membrane was concluded from inhibitor profiles, zymography, and the apparent molecular mass values and hydrophobicity of the fibrinogen degradation products that it generated, to be the composite action of the azurophil granule proteases, human neutrophil elastase, cathepsin G and possibly proteinase 3. Electron microscopy analysis of PMA stimulated neutrophils incorporated within fibrin clots revealed morphological changes suggestive of neutrophil degranulation, and the proteolytic activity released by these cells was shown to be identical to that of azurophil granule proteases with respect to the apparent molecular mass values of the fibrin products that it generated. Immunoelectron microscopy revealed minimal internalization of fibrin like material during this process suggesting that neutrophil mediated fibrinolysis under these conditions is predominantly an extracellular event. Immunoelectron microscopy was used to localise fibrinogen degradation products previously reported to be associated with the neutrophil following incubation with fibrinogen. This revealed neutrophil associated fibrinogen products to be intracellular. Internalisation appears to be the result of pinocytosis which is stimulated in the presence of PMA. Although internalisation may be enhanced by an initial interaction of fibrinogen with the neutrophil membrane, a large proportion of uptake occurs via the fluid phase. Both intact and degraded forms of fibrinogen can associate with the neutrophil. Internalised material is rapidly degraded intracellularly into low molecular weight products which are partially released into the surrounding medium. This intracellular degradation, however, contributes minimally to the overall degradation of fibrinogen by neutrophils; the major pathway is extracellular. The demonstration in this· study, that the previously identified fibrinogen- fibrin- and CRP-degrading activity of the neutrophil membrane is due to azurophil granule proteases co-incides with numerous recent reports suggesting that membrane bound forms of these proteases, due to their ability to evade naturally occurring protease inhibitors, are the biologically relevant forms of these proteases. The membrane expression of azurophil granule proteases has recently been shown to be under the control of a variety of inflammatory mediators. Thus, neutrophil mediated degradation of fibrinogen, fibrin and CRP in vivo may be tightly controlled by the regulated expression of azurophil granule proteases on the neutrophil membrane.
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Hoenderdos, Kim. "Modulation of neutrophil degranulation by hypoxia." Thesis, University of Cambridge, 2015. https://www.repository.cam.ac.uk/handle/1810/247459.

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Neutrophils are key effector cells of the innate immune system. They employ a number of powerful ‘weapons’ to eliminate pathogens, including an array of destructive proteins packaged into distinctive granule subsets. In addition to their microbicidal activity, these granule proteins are capable of causing substantial tissue damage if inappropriately deployed. To mitigate against this possibility, most physiological stimuli induce minimal extracellular degranulation. Sites of inflammation and infection are usually hypoxic, and it has been shown that oxygen depletion compromises neutrophil function by impairing the generation of reactive oxygen species and hence bacterial killing. The key finding reported in this thesis is that hypoxia substantially increases the release of all neutrophil granule subsets, as measured by the release of (active) hallmark proteins (elastase, myeloperoxidase, lactoferrin and matrix metalloproteinase-9). In consequence, supernatants from hypoxic neutrophils induced substantially more damage to lung epithelial cell layers than supernatants from neutrophils cultured under normoxic conditions; this damage was protein- and protease-dependent. This pattern of damage was seen consistently across lung adenocarcinoma-derived epithelial cells, primary immortalised lung epithelial cells, and primary human bronchial epithelial cells grown in physiological air-liquid interface culture. Surprisingly, the mechanism of hypoxia-augmented degranulation was found to be independent of protein synthesis and specifically, of the transcription factor HIF-1α (the ‘master-regulator’ of hypoxic responses); thus, hypoxia did not affect mRNA transcript or protein abundance of the major granule components, and hypoxia mimetics failed to recapitulate the phenotype. Inhibition of the key pathways known to be involved in neutrophil degranulation, including, phosphatidylinositol 3-kinase and phospholipase C, but not calcium flux prevented augmented granule release under hypoxia In conclusion, hypoxia induces a destructive neutrophil phenotype, with increased release of multiple histotoxic proteases. This may contribute to tissue injury and disease pathogenesis in a range of clinically important conditions.
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Chen, Justin. "The effect of hyperleptinemia on polymorphonuclear neutrophil-endothelial interactions /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101709.

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Obesity is a growing major public health concern and is associated with various co-morbidities. Given recent evidence of increased bacterial infections in bariatric patients, morbid obesity may adversely affect the immune system. As a pleiotropic pro-inflammatory mediator produced primarily by adipocytes, leptin is a link between metabolism and immunity. Consequently, excessive leptin secretion may hinder the body's ability to defend against bacterial infection. This situation arises in morbid obesity, where chronic hyperleptinemia is observed. We used an in vivo murine model of hyperleptinemia to determine whether abnormal levels of circulating leptin have a detrimental effect on the trafficking of neutrophils, with respect to the number present, their rolling velocity, preadherence, and adherence to the endothelium.
Male CD1 background mice (6-8 weeks) were divided to 3 treatment groups receiving once daily ip injections (1) sham (PBS); (2) low leptin (1mug/g); (3) high leptin (5mug/g). After 7 days of treatment, intravital microscopy was used to visualize post-capillary venule microcirculation of the cremaster muscle in the scrotum. Parameters such as neutrophil rolling, rolling velocity, preadherence, and adherence, were recorded and measured to assess PMN kinetics.
High doses of leptin resulted in increased preadherence and adherence of neutrophils in post-capillary venules. Serum leptin and TNFalpha levels were found not to correlate with this observation; consequently, potential pathways through which leptin increases PMN adhesion could not be elucidated. Conceivably, excessive adhesion could adversely affect neutrophil trafficking by producing a shift towards the marginal pool, limiting their ability to appropriately home into bacterial targets. This could parallel the situation in morbid obesity where high concentrations of leptin are also observed.
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Boespflug, Nicholas. "ATF3 regulates neutrophil migration in mice." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1382372804.

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Lin, Yongqing. "Study of neutrophil diapedesis across a bovine mammary epithelium in vitro." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=22761.

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Bovine mastitis due to bacterial infection is one of the most costly diseases affecting the dairy industry. The polymorphonuclear neutrophils (PMNs) present in milk have a central protective role against invading pathogens, However, the manner by which PMNs traverse the secretory epithelia and the relationship between PMN diapedesis and the epithelial damage are unclear. This in vitro study investigated the process and rate of bovine PMN transepithelial migration. The bovine mammary epithelial cell line, MAC-T, formed a confluent monolayer with characteristic tight junctions, polarity and functional barrier to the dye trypan blue. In the first series of experiments, neutrophils were added into the upper compartment of the culture insert and stimulated to migrate across the epithelium in an apical-to-basal direction by the addition of Staphylococcus aureus to the lower compartment. Light and transmission electron microscopy revealed the following series of events for PMN transmigration: (1) adherence of PMNs to the surface of the epithelium; (2) projection of pseudopods toward the intercellular junction; (3) migration between adjacent epithelial cells; and (4) re-approximation of epithelial cell membranes and reformation.
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Chung, Henry Hung Li. "Engineered Microenvironment for Quantitative Studies of Neutrophil Migration." Thesis, University of Rochester, 2015. http://pqdtopen.proquest.com/#viewpdf?dispub=3686523.

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Cell migration is present in virtually all life processes, including fertilization, embryogenic development, immune response, wound healing, and tumor metastasis. To improve the treatment of diseases associated with these various life processes, it is important to understand the underlying mechanisms of cell migration involved. This often requires that we recreate the environment that leads to and supports the continuous migration of cells. Here, we present two engineering approaches toward such a goal, with the additional emphasis that cell migration can be conducted in the absence of fluid flow, a mechanical stimulus that is known to influence cell behaviors. We chose the primary human neutrophil, which is highly motile and sensitive to both fluid flow and chemoattraction, as the model cell type for all our studies.

In the first approach, we used fluid flow to create a linear and time-invariant gradient of chemoattractants to guide the migration of neutrophils. A thin and porous membrane was used to screen off the associated flow forces while still permitting the diffusion of the gradient to the neutrophils. We showed that the membrane-based system is capable of directing neutrophil migration without the bias from fluid flow, and allowed within minutes the exchange of media to label and wash the migrated neutrophils. To assess the reduction of flow forces enabled by the membrane, we developed an analytical model to predict the direction and the magnitude of flow within the system. The validity of the model was verified both experimentally and numerically with particle tracking and computational fluid mechanic (CFM) simulations. We also performed total internal reflection fluorescence (TIRF) microscopy to verify the preservation of the gradient after v its diffusion through the membrane.

In the second approach, we created immobilized gradients of the chemoattractant interleukin 8 (IL-8) and the intercellular adhesion molecule 1 (ICAM-1) in the attempt to guide neutrophil migration. A gradient of soluble factors is first established, and the resulting difference of concentration over space leads to a bias in the binding of the soluble factors unto the substrate, forming an immobilized gradient. The immobilization is mediated by a combination of different physicochemical linkages, including electrostatic attraction, protein/protein interactions, and covalent bonding. We showed through labeling with fluorescent antibody that the number of IL-8 or ICAM-1 immobilized in a given area could be controlled, and varied over distances to form different gradient profiles. We further showed that our immobilization procedure does not affect the ability of IL-8 and ICAM-1 to activate and bind the neutrophils. However, with all the immobilized gradients that we have created so far, none were able to effectively promote the directed migration of neutrophils in long distances. Additional work is therefore required to establish if an immobilized gradient of either IL-8 or ICAM-1 alone can direct the migration of neutrophils in long distances, and if it does, what are the required conditions. Currently, our efforts suggest that the membrane-based chemotaxis system is a more attainable platform for promoting a directed migration that is shear-free.

The presented thesis work offers many potential applications. The membrane-based chemotaxis system, which has the general structure of two compartments separated by a membrane, resembled many physiological structures, including bone marrow, blood vessel, blood-brain barrier, hepatic portal vein, nephron in the kidneys, and alveolus in vi the lungs, and therefore serves as a versatile platform for understanding the transport phenomenon and the biochemical signaling in the aforementioned tissues. With improvements, the membrane-based system can also host larger-scale cell culture for protein production and tissue engineering. The protocols established for the gradient immobilization also provided many valuable references. These include: 1. A 1st order approximation of the reagents and the times required to fully saturate the substrate to be functionalized. 2. An automated image processing tool to measure the various parameters of cell motility. 3. A statistical framework to detect the presence of a directed migration. In theory, the standard operating procedures established are applicable to the surface functionalization with other peptides and proteins.

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Books on the topic "Immunology, Neutrophil"

1

A, Metcalf Julia, ed. Laboratory manual of neutrophil function. New York: Raven Press, 1986.

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Lilliehook, Inger. Studies of blood eosinophil and neutrophil granulocytes in health and diseased dogs. Uppsala: Sveriges Lantbruksuniversitet, 1999.

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Berezhnai͡a, N. M. Neĭtrofily i immunologicheskiĭ gomeostaz. Kiev: Nauk. dumka, 1988.

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Alonso-Fernández, Patricia. Neutrophils in biological age and longevity. New York: Nova Science Publishers, Inc., 2011.

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The Neutrophil: An Emerging Regulator of Inflammatory and Immune Response (Chemical Immunology). Not Avail, 2003.

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DeLeo, Frank, and Mark T. Quinn. Neutrophil: Methods and Protocols. Springer, 2019.

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DeLeo, Frank R., and Mark T. Quinn. Neutrophil: Methods and Protocols. Springer, 2020.

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Marzano, Angelo Valerio, Dan Lipsker, and Massimo Cugno, eds. Neutrophil-mediated skin diseases: immunology and genetics. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88963-254-1.

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Immunopharmacology of neutrophils. London: Academic Press, 1994.

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Hellewell, Paul G., Clive Page, and Timothy J. Williams. Immunopharmacology of Neutrophils. Elsevier Science & Technology Books, 1994.

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Book chapters on the topic "Immunology, Neutrophil"

1

Dockrell, David H., Emmet E. McGrath, Moria K. B. Whyte, and Ian Sabroe. "The Neutrophil." In Immunology of Fungal Infections, 51–73. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/1-4020-5492-0_3.

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Edwards, S. W., D. A. Moulding, M. Derouet, and R. J. Moots. "Regulation of Neutrophil Apoptosis." In Chemical Immunology and Allergy, 204–24. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000071562.

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Holland, Steven M. "Neutropenia and Neutrophil Defects." In Manual of Molecular and Clinical Laboratory Immunology, 766–74. Washington, DC, USA: ASM Press, 2016. http://dx.doi.org/10.1128/9781555818722.ch78.

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Uciechowski, Peter, and Lothar Rink. "Basophil, Eosinophil, and Neutrophil Functions in the Elderly." In Immunology of Aging, 47–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-39495-9_5.

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Baggiolini, M., A. Walz, T. Brunner, B. Dewald, V. von Tscharner, R. Zwahlen, C. Dahinden, et al. "Novel Neutrophil-Activating Peptides and Their Role in Inflammation." In Progress in Immunology, 765–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83755-5_104.

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Hannigan, M. O., C. K. Huang, and D. Q. Wu. "Roles of PI3K in Neutrophil Function." In Current Topics in Microbiology and Immunology, 165–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18805-3_6.

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Sha’afi, R. I., and T. F. P. Molski. "Activation of the Neutrophil (Part 1 of 4)." In Chemical Immunology and Allergy, 1–16. Basel: KARGER, 1988. http://dx.doi.org/10.1159/000318681.

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Sha’afi, R. I., and T. F. P. Molski. "Activation of the Neutrophil (Part 2 of 4)." In Chemical Immunology and Allergy, 17–32. Basel: KARGER, 1988. http://dx.doi.org/10.1159/000318683.

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Sha’afi, R. I., and T. F. P. Molski. "Activation of the Neutrophil (Part 3 of 4)." In Chemical Immunology and Allergy, 33–49. Basel: KARGER, 1988. http://dx.doi.org/10.1159/000318684.

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Sha’afi, R. I., and T. F. P. Molski. "Activation of the Neutrophil (Part 4 of 4)." In Chemical Immunology and Allergy, 50–64. Basel: KARGER, 1988. http://dx.doi.org/10.1159/000318685.

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Conference papers on the topic "Immunology, Neutrophil"

1

Wu, Julie, Anne Pipathsouk, A. Keizer-Gunnink, Wynand Alkema, Fabrizia Fusetti, Shanshan Liu, Steve Atschuler, Lani Wu, Arjan Kortholt, and Orion Weiner. "Abstract B48: Homer3 regulates the establishment of neutrophil polarity." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b48.

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Kumagai, Yuko, Rihito Kanamaru, Hideyuki Ohzawa, Hisanaga Horie, Yoshinori Hosoya, Naohiro Sata, and Joji Kitayama. "Abstract B77: Low-density neutrophils (LDN) in circulating blood of postoperative patients may participate in the development of distant recurrence through the production of neutrophil extracellular traps (NETs)." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-b77.

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Yazdani, Hamza O., Christof T. Kaltenmeier, David Geller, and Samer Tohme. "Abstract A97: Neutrophil extracellular traps (NETs) promote immune escape and metastatic growth after surgical stress." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a97.

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Mollaoglu, Gurkan, Alex Jones, Sarah Wait, Anandaroop Mukhopadhyay, Sangmin Jeong, Rahul Arya, Soledad Camolotto, et al. "Abstract B72: Lineage specifiers SOX2 and NKX2-1 inversely regulate tumor cell fate and neutrophil recruitment in lung cancer." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-b72.

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Seitz, R., M. Wolf, R. Egbring, and K. Havemann. "Neutrophil Elastase, Thrombin and Plasmin in Septic Shock: Influence on Prognosis." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643894.

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The prognosis of septicaemia depends on the occurrence of disseminated disturbances of the microcirculation impairing organ function and haemorrhagic complications due to consumption of coagulation factors. The intravasal appearance of three potentially involved proteinases in active form can be detected by immunologic determination of their complexes with inhibitors: thrombin-antithrombin III (TAT), according to PELZER et al. (Thrombos. Haemostas. 54:24,1985); plasmin- antiplasmin (PAP), ldlE, antiserum donated by KARGES; human neutrophil elastase (HNE)- antitrypsin, ELISA, Merck, DarmstadtIn 47 patients with septic shock (19 survived, group A; 28 lethal, group B) the PAP levels were moderately elevated throughout the course without vaviations related to the outcome. TAT was initially strongly increased in both groups (18.8±6.3 ng/ml/16.5±7.2), and decreased towards the end of the course in both groups (2.7±0.5/3.7±0.8). Though the intial HNE levels were higher in group A (2458±348ng/ml) than in group B (1291±295, p=0.017), they decreased, in group A more rapidly and were at the end almost significantly lower than in group B (315±54/652&3x00B1;161, p=0,059). The decrease of TAT as well as HNE was associated with substitution of antithrombin III concentate (ATIII) and fresh frozen plasma (ffp) given with the aim of normalization of haemostasis and replacement of inhibitors. Factor XIII, a substrate of both thrombin and HNE, was initially equally low about 50% of normal in both groups, but increased only in group A (69.1±7.1/49.6±5.5, p=0.045) towards the end.Conclusions: Both TAT and HNE decreased after initial elevation under substitution of ATIII and ffp. A rapid decrease seems to be a favourable sign which is accompanied by rising levels of F XIII, while sustained elevation of HNE points to a poor prognosis
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Rayes, Roni F., Alexandra Tinfow, Dorothy Antonatos, France Bourdeau, Betty Giannias, and Jonathan D. Spicer. "Abstract B41: Neutrophils modulate T-cell recruitment and promote hepatic metastases in lung cancer." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-b41.

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Mishalian, Inbal, Rachel Bayuh, Lida Zolotarov, Liran Levy, Sunil Singhal, Steven M. Albelda, and Zvi Gregorio Fridlender. "Abstract A68: Tumor-associated neutrophils (TAN) develop protumorigenic properties during tumor progression." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-a68.

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Sippel, Trisha R., Rae Russell, Timothy Ung, Marci Klaassen, and Allen Waziri. "Abstract A44: Disrupted transmigration of neutrophils in glioblastoma patients is augmented by steroid treatment." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-a44.

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Herbst, Brian, Elizabeth Jaffee, and Lei Zheng. "Abstract PR10: Inhibition of MEK1/2 overcomes resistance to aPD-1 blockade in pancreatic ductal adenocarcinoma through modulation of NETosis in tumor-associated neutrophils." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 5-6, 2021. American Association for Cancer Research, 2022. http://dx.doi.org/10.1158/2326-6074.tumimm21-pr10.

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Perobelli, Suelen Martins, Ana Carolina Terra Mercadante, Triciana Gonçalves-Silva, Rômulo Galvani, Antônio Pereira-Neves, Marlene Benchimol, Alberto Nobrega, and Adriana Bonomo. "Abstract B39: Neutrophils G-CSF stimulated promotes specific protection against graft vs. host disease and keeps the graft vs. leukemia effect." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b39.

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