scholarly journals Response of Human Neutrophil Granulocytes to the Hyphae of the Emerging Fungal Pathogen Curvularia lunata

Pathogens ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 235
Author(s):  
Eszter Judit Tóth ◽  
Mónika Varga ◽  
Miklós Takó ◽  
Mónika Homa ◽  
Olivér Jáger ◽  
...  
Keyword(s):  
Oxidative Burst ◽  
Human Neutrophil ◽  
Fungal Pathogen ◽  
Fungal Infections ◽  
Neutrophil Function ◽  
Neutrophil Extracellular Trap ◽  
Curvularia Lunata ◽  
Neutrophil Granulocytes ◽  
Infectious Agents ◽  
First Line

Curvularia lunata is an ascomycete filamentous fungus causing local and invasive phaeohyphomycoses in both immunocompromised and immunocompetent patients. Neutrophils are crucial participants of the first line host defense against fungal infections. They migrate to the infected site and eliminate the infectious agents by various mechanisms including phagocytoses, oxidative damage, or formation of neutrophil extracellular trap (NET). Neutropenia may be a risk factor for phaeohyphomycoses, and restoration of the neutrophil function can improve the outcome of the infection. In the present study, interaction of primary human neutrophil granulocytes with the hyphae C. lunata was examined and compared to that with the well characterized filamentous fungal pathogen Aspergillus fumigatus. Neutrophils could recognize the serum opsonized hyphae of C. lunata and attach to them. Myeloperoxidase release was also activated by a soluble factor present in the culture supernatant of the fungus. Induction of the oxidative burst was found to depend on serum opsonization of the hyphae. Although extracellular hydrogen peroxide production was induced, the fungus efficiently blocked the oxidative burst by acidifying the reaction environment. This blockage also affected the NET forming ability of the neutrophils.

scholarly journals Immobilized Immune Complexes Induce Neutrophil Extracellular Trap Release by Human Neutrophil Granulocytes via FcγRIIIB and Mac-1

2014 ◽  
Vol 193 (4) ◽  
pp. 1954-1965 ◽  
Author(s):  
Martina Behnen ◽  
Christoph Leschczyk ◽  
Sonja Möller ◽  
Tobit Batel ◽  
Matthias Klinger ◽  
...  
Keyword(s):  
Immune Complexes ◽  
Human Neutrophil ◽  
Neutrophil Extracellular Trap ◽  
Neutrophil Granulocytes ◽  
Extracellular Trap

Study of neutrophil function in different age group

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Sherein Mohamed Rashad ◽  
Fawzeia Hassan Ahmed Aboali ◽  
Mohamed Nazmy Fares ◽  
Rasha Yousef Shahin ◽  
Amira Ramadan Elmahdi
Keyword(s):  
Immune System ◽  
Fluorescence Intensity ◽  
Oxidative Burst ◽  
Effector Cell ◽  
Descriptive Study ◽  
Neutrophil Function ◽  
Age Group ◽  
First Line ◽  
Cross Sectional ◽  
Immunological Status

Abstract Background Neutrophils are the body's first line of defense against microorganisms, and a critical effector cell in both innate and humoral immunity. The immune system experiences profound changes with aging, thereby increasing the susceptibility to infectious diseases. Neutrophils from aged hosts consistently show impairments in the phagocytosis of opsonized bacteria, and the ability to kill phagocytosed microorganisms. Objectives determine oxidative burst function of neutrophil in in different age group. Methods cross sectional descriptive study, carried out in obesity clinic Ain shams university Results we found that Peak fluorescence intensity results is 95.5±2.6 in age group 20-40yr, 94.8±2.6 in age group 41-60yr and 86,8±15.1 in age group ≥61yr.The Percent neutrophil stimulation is 74.2 ±10 in age group 20-40yr, 74.8±9.2 in age group 41-60yr and 69.6± in age group ≥61yr . Conclusion and Recommendation there is a slight decreased in the peak fluorescence intensity and the Percent neutrophil stimulation with ageing. We recommend more healthcare of elderly to improve their immunological status.

Effects of gadolinium oxide nanoparticles on the oxidative burst from human neutrophil granulocytes

2012 ◽  
Vol 23 (27) ◽  
pp. 275101 ◽  
Author(s):  
Natalia Abrikossova ◽  
Caroline Skoglund ◽  
Maria Ahrén ◽  
Torbjörn Bengtsson ◽  
Kajsa Uvdal
Keyword(s):  
Oxidative Burst ◽  
Human Neutrophil ◽  
Gadolinium Oxide ◽  
Oxide Nanoparticles ◽  
Neutrophil Granulocytes ◽  
Gadolinium Oxide Nanoparticles

scholarly journals Increased peripheral blood neutrophil activation phenotypes and NETosis in critically ill COVID-19 patients

2021 ◽  
Author(s):  
Jorge A. Masso-Silva ◽  
Alexander Moshensky ◽  
Michael T. Y. Lam ◽  
Mazen Odish ◽  
Arjun Patel ◽  
...  
Keyword(s):  
Disease Severity ◽  
Critically Ill ◽  
Oxidative Burst ◽  
Ex Vivo ◽  
Inflammatory Diseases ◽  
Lung Parenchyma ◽  
Neutrophil Function ◽  
Neutrophil Extracellular Trap ◽  
Peripheral Blood Neutrophil ◽  
Cytokine Levels

AbstractBackgroundIncreased inflammation is a hallmark of COVID-19, with pulmonary and systemic inflammation identified in multiple cohorts of patients. Definitive cellular and molecular pathways driving severe forms of this disease remain uncertain. Neutrophils, the most numerous leukocytes in blood circulation, can contribute to immunopathology in infections, inflammatory diseases and acute respiratory distress syndrome (ARDS), a primary cause of morbidity and mortality in COVID-19. Changes in multiple neutrophil functions and circulating cytokine levels over time during COVID-19 may help define disease severity and guide care and decision making.MethodsBlood was obtained serially from critically ill COVID-19 patients for 11 days. Neutrophil oxidative burst, neutrophil extracellular trap formation (NETosis), phagocytosis and cytokine levels were assessed ex vivo. Lung tissue was obtained immediately post-mortem for immunostaining.ResultsElevations in neutrophil-associated cytokines IL-8 and IL-6, and general inflammatory cytokines IP-10, GM-CSF, IL-1b, IL-10 and TNF, were identified in COVID-19 plasma both at the first measurement and at multiple timepoints across hospitalization (p < 0.0001). Neutrophils had exaggerated oxidative burst (p < 0.0001), NETosis (p < 0.0001) and phagocytosis (p < 0.0001) relative to controls. Increased NETosis correlated with both leukocytosis and neutrophilia. Neutrophils and NETs were identified within airways and alveoli in the lung parenchyma of 40% of SARS-CoV-2 infected lungs. While elevations in IL-8 and ANC correlated to COVID-19 disease severity, plasma IL-8 levels alone correlated with death.ConclusionsCirculating neutrophils in COVID-19 exhibit an activated phenotype with increased oxidative burst, NETosis and phagocytosis. Readily accessible and dynamic, plasma IL-8 and circulating neutrophil function may be potential COVID-19 disease biomarkers.

scholarly journals Primary immune deficiencies with defects in neutrophil function

Hematology ◽  
2016 ◽  
Vol 2016 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Mary C. Dinauer
Keyword(s):  
Fungal Infections ◽  
Leukocyte Adhesion ◽  
Genetic Disorders ◽  
Clinical Manifestations ◽  
Treatment Strategies ◽  
Adaptor Protein ◽  
Invasive Fungal Disease ◽  
Neutrophil Function ◽  
Microbial Pathogens ◽  
Immune Deficiencies

Abstract Immune deficiencies resulting from inherited defects in neutrophil function have revealed important features of the innate immune response. Although sharing an increased susceptibility to bacterial and fungal infections, these disorders each have distinctive features in their clinical manifestations and characteristic microbial pathogens. This review provides an update on several genetic disorders with impaired neutrophil function, their pathogenesis, and treatment strategies. These include chronic granulomatous disease, which results from inactivating mutations in the superoxide-generating nicotinamide dinucleotide phosphate oxidase. Superoxide-derived oxidants play an important role in the control of certain bacterial and fungal species, and also contribute to the regulation of inflammation. Also briefly summarized are updates on leukocyte adhesion deficiency, including the severe periodontal disease characteristic of this disorder, and a new immune deficiency associated with defects in caspase recruitment domain–containing protein 9, an adaptor protein that regulates signaling in neutrophils and other myeloid cells, leading to invasive fungal disease.

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