[Influence of Solcotrichovac vaccine on formation of neutrophil extracellular traps].
DolgushinAndreeva IuSRyzhkova AiSavochkina AIuMezentseva EaNikushkina KvО. С. АбрамовскихMarachev SiMatveeva Dn
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To study the influence of Solcotichovac vaccine on formation of neutrophil extracellular traps.Solcotrichovac vaccine administered in various doses was used in order to assess the formation of neutrophil extracellular traps in peripheral blood of women of childbearing age.Therapeutic dose of Solcotrichovac stimulated the most prominent formation of neutrophil extracellular traps.Solcotrichovac vaccine stimulated non-specific arm of mucosal immunity due to formation of neutrophil extracellular traps and it is probable that this mechanism explains the effect of this vaccine.Keywords:
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Polymorphonuclear neutrophils( PMNs)are one of the first defenses against invading microbes.There are two ways for PMNs to kill bacteria,phagocytosis and neutrophil extracellular traps( NETs),which is much more effective.NETs are composed of DNA and protein.After the stimulation of inducing factor,NETs appear and capture the pathogens.The mechanism of NETs becomes a current research focus in the field of PMNs.
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The respiratory burst of neutrophils is an important response in inflammation. The alterations in extracellular pH per se is not a sufficient trigger to the respiratory burst in neutrophils. While neutrophils in respose to conventional agonists, the respiratory burst in neutrophils is affected by the alterations in extracellular pH, and there is a direct relationship between intracellular and extracellular pH. O-· 2 production in neutrophils is decreased while H 2O 2 production is increased at acidic pH. O-· 2 release in neutrophils is enhanced at weak alkaline pH. Na+/H+ exchanger plays an important role in the regulation of the respiratory burst of neutrophils.
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Abstract Neutrophil extracellular traps are associated with a unique form of cell death distinct from apoptosis or necrosis, whereby invading microbes are trapped and killed. Neutrophil extracellular traps can contribute to autoimmunity by exposing autoantigens, inducing IFN-α production, and activating the complement system. The association of neutrophil extracellular traps with autoimmune diseases, particularly systemic lupus erythematosus, will be reviewed. Increased neutrophil extracellular trap formation is seen in psoriasis, antineutrophil cytoplasmic antibody-associated vasculitis, antiphospholipid antibody syndrome rheumatoid arthritis, and systemic lupus erythematosus. Neutrophil extracellular traps may promote thrombus formation in antineutrophil cytoplasmic antibody-associated vasculitis and antiphospholipid antibody syndrome. In systemic lupus erythematosus, increased neutrophil extracellular trap formation is associated with increased disease activity and renal disease, suggesting that neutrophil extracellular traps could be a disease activity marker. Neutrophil extracellular traps can damage and kill endothelial cells and promote inflammation in atherosclerotic plaques, which may contribute to accelerated atherosclerosis in systemic lupus erythematosus. As neutrophil extracellular traps induce IFN-α production, measuring neutrophil extracellular traps may estimate IFN-α levels and identify which systemic lupus erythematosus patients have elevated levels and may be more likely to respond to emerging anti-IFN-α therapies. In addition to anti-IFN-α therapies, other novel agents, such as N-acetyl-cysteine, DNase I, and peptidylarginine deiminase inhibitor 4, target neutrophil extracellular traps. Neutrophil extracellular traps offer insight into the pathogenesis of autoimmune diseases and provide promise in developing disease markers and novel therapeutic agents in systemic lupus erythematosus. Priority areas for basic research based on clinical research insights will be identified, specifically the potential role of neutrophil extracellular traps as a biomarker and therapeutic target in systemic lupus erythematosus.
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Trauma increases susceptibility to secondary bacterial infections. The events suppressing antimicrobial immunity are unclear. Polymorphonuclear neutrophils (PMNs) migrate toward bacteria using chemotaxis, trap them in extracellular neutrophil extracellular traps, and kill them using respiratory burst (RB). We hypothesized that plasma and wound fluids from trauma patients alter PMN function.Volunteer PMNs were incubated in plasma or wound fluids from trauma patients (days 0 and 1, days 2 and 3), and their functions were compared with PMNs incubated in volunteer plasma. Chemotaxis was assessed in transwells. Luminometry assessed total and intracellular RB responses to receptor-dependent and independent stimulants. Neutrophil extracellular trap formation was assessed using elastase assays. The role of tissue necrosis in creating functionally suppressive systemic PMN environments was assessed using a novel pig model where PMNs were incubated in uninjured pig plasma or plasma from pigs undergoing intraperitoneal instillation of liver slurry.Both plasma and wound fluids from trauma patients markedly suppress total PMN RB. Intracellular RB is unchanged, implicating suppression of extracellular RB. Wound fluids are more suppressive than plasma. Biofluids suppressed RB maximally early after injury and their effects decayed with time. Chemotaxis and neutrophil extracellular trap formation were suppressed by biofluids similarly. Lastly, plasma from pigs undergoing abdominal liver slurry instillation suppressed PMN RB, paralleling suppression by human trauma biofluids.Trauma plasma and wound fluids suppress RB and other key PMNs antimicrobial functions. Circulating suppressive signals can be derived from injured or necrotic tissue at wound sites, suggesting a key mechanism by which tissue injuries can put the host at risk for infection.
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To study the influence of Solcotichovac vaccine on formation of neutrophil extracellular traps.Solcotrichovac vaccine administered in various doses was used in order to assess the formation of neutrophil extracellular traps in peripheral blood of women of childbearing age.Therapeutic dose of Solcotrichovac stimulated the most prominent formation of neutrophil extracellular traps.Solcotrichovac vaccine stimulated non-specific arm of mucosal immunity due to formation of neutrophil extracellular traps and it is probable that this mechanism explains the effect of this vaccine.
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Neutrophils phagocytose and kill microbes upon phagolysosomal fusion. Recently we found that activated neutrophils form extracellular fibres that consist of granule proteins and chromatin. These neutrophil extracellular traps (NETs) degrade virulence factors and kill Gram positive and negative bacteria. Here we show for the first time that Candida albicans, a eukaryotic pathogen, induces NET-formation and is susceptible to NET-mediated killing. C. albicans is the predominant aetiologic agent of fungal infections in humans, particularly in immunocompromised hosts. One major virulence trait of C. albicans is its ability to reversibly switch from singular budding cells to filamentous hyphae. We demonstrate that NETs kill both yeast-form and hyphal cells, and that granule components mediate fungal killing. Taken together our data indicate that neutrophils trap and kill ascomycetous yeasts by forming NETs.
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