Publications by authors named "Michal Pruchniak"

Acute leukemias, the most common cancers in children, are characterized by excessive proliferation of malignant progenitor cells. As a consequence of impaired blood cell production, leukemia patients are susceptible to infectious complications-a major cause of non-relapse mortality. Neutrophil extracellular traps (NETs) are involved in various pathologies, from autoimmunity to cancer.

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Neutrophils are one of the first cells to arrive at the site of infection, where they apply several strategies to kill pathogens: degranulation, respiratory burst, phagocytosis, and release of neutrophil extracellular traps (NETs). Recent discoveries try to connect NETs formation with autoimmune diseases, like systemic lupus erythematosus (SLE) or granulomatosis with polyangiitis (GPA) and place them among one of the factors responsible for disease pathogenesis. The aim of the study was to assess the NETotic capabilities of neutrophils obtained from freshly diagnosed autoimmune patients versus healthy controls.

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Introduction: NETosis is a process whereby neutrophils release chromatin into the surrounding extracellular matrix to form neutrophil extracellular traps (NETs). Under physiological conditions NETosis can be initiated by a variety of stimuli, including immune complexes, complement activation products, and a milieu of proinflammatory cytokines. Because overproduction of NETs is often related to the promotion or aggravation of autoimmune responses, we decided to assess how simultaneous activation of NETosis by different stimuli affects NET production.

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A unique strategy, in which invading microorganisms are being caught in web-like structures composed mainly of DNA, involves a recently described phenomenon called NETosis. This process seems to be related to the production of reactive oxygen species (ROS). In our study, the influence of diphenyleneiodonium chloride (DPI), which diminishes ROS production, was assessed in the context of neutrophil extracellular trap (NET) release.

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Friend or foe? This is often asked question when it comes to neutrophil extracellular traps studies. There is no simple answer to that. At the time of their discovery they were considered to be protectors of our well-being.

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Generation of reactive oxygen species is a physiological process that take place in every aerobic organism. Oxidative stress is defined as a disturbance in the balance between the production of free radicals and antioxidants in favor of the oxidants. The imbalance between those two fractions may potentially lead to cell damage at molecular level.

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When pathogens invade the body, neutrophils create the first line of defense. Basic weaponry consists of phagocytosis and degranulation, but these cells have yet another ace in the sleeve, a unique strategy in which invading microorganisms are being destroyed. These cellular warriors are able to release nuclear chromatin and form extracellular structure, known as neutrophil extracellular traps (NET).

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Neutrophils are among the first responders to virulent factors. They kill microbes by phagocytosis, oxidative burst, and as neutrophil extracellular traps (NETs). NETs production leads to unique cell death depending on, inter alia, reactive oxygen species (ROS).

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Neutrophils are one of the main types of effector cells in the innate immune system. Neutrophils play a major role in fighting diseases and are recruited almost immediately to sites of infection. The neutrophils have a variety of defensive mechanisms and their high affinity to chemotactic agents makes them ideal in the defense against pathogens.

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NETosis is a unique death pathway that differs from apoptosis and necrosis and depends on the generation of reactive oxygen species (ROS) by NADPH oxidase. During this process, neutrophil extracellular traps (NETs) are created. NETs are extracellular structures composed of chromatin and variety of proteins from cells granules that bind and kill microorganisms.

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