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Neutrophil extracellular traps

In previous work we have shown the possibility of detecting an immune defense reaction called the formation of Neutrophil Extracellular Traps (NETs) by impedance spectroscopy on cell cultures [2], [3]. These chromatin structures are released by neutrophils, one kind... [Pg.15]

Keywords neutrophil granulocytes, impedance spectroscopy, interdigitated electrodes, neutrophil extracellular traps, biological cells... [Pg.65]

Clark, S., A. Ma, S. Tavener, B. McDonald, Z. Goodatzi, M. Kelly, K. Patel, S. Chakrabarti, E. McAvoy, G. Sinclair, et al. (2007). Platelet tlr4 activates neutrophil extracellular traps to ensnare bacteria in... [Pg.69]

ABSTRACT Neutrophil granulocytes play an important role in the human immune defence. One of their weapons against bacteria and fungi is the release of Neutrophil Extracellular Traps (NETs) which form in great amounts a biofilm. Electrical Impedance Spectroscopy (EIS) enables the examination of the NET-formation to determine the reaction parameters and to investigate the state of wound inflammation. In this work we analyze the behaviour of neutrophils in vitro and develop an empiric model of the states of NET-formation. This model can be used to develop a wound sensor which monitors the NET-formation caused by an infection in vivo. [Pg.59]

Keywords. Neutrophil Extracellular Traps, bioimpedance, dielectric cell properties, wound... [Pg.59]

Caudrillier A, Kessenbrock K, GilKss BM, Nguyen JX, Marques MB, Monestier M, et al. Platelets induce neutrophil extracellular traps in... [Pg.498]

Figure 2. (1) Neutrophils circulating passively in blood capillary. (2) Chemoattractants may be detected by the circulating neutrophils, by the endothelial cells lining the lumen, or both in order that the neutrophils become adhesive. This adhesion is mediated by selectins, a group of cell surface proteins. Neutrophils roll on the surface of the endothelial cells and then actively locomote seeking out spaces between the endothelial cells. (3) The adhesive neutrophils begin to squeeze between endothelial cells. (4) Cells move through the extracellular matrix towards the site of infection. Here adhesion is low and may not be necessary for locomotion. (5) At the site of infection, neutrophils become trapped by increased adhesion where they phagocytose bacteria and liberate the contents of their granules. After Lackie (1982,1986). Figure 2. (1) Neutrophils circulating passively in blood capillary. (2) Chemoattractants may be detected by the circulating neutrophils, by the endothelial cells lining the lumen, or both in order that the neutrophils become adhesive. This adhesion is mediated by selectins, a group of cell surface proteins. Neutrophils roll on the surface of the endothelial cells and then actively locomote seeking out spaces between the endothelial cells. (3) The adhesive neutrophils begin to squeeze between endothelial cells. (4) Cells move through the extracellular matrix towards the site of infection. Here adhesion is low and may not be necessary for locomotion. (5) At the site of infection, neutrophils become trapped by increased adhesion where they phagocytose bacteria and liberate the contents of their granules. After Lackie (1982,1986).
Figure 6.11. Intracellular Ca2+ levels during neutrophil activation with fMet-Leu-Phe. Neutrophil suspensions were loaded with Fluo-3 AM for 15 min. This molecule is membrane permeable but cleaved by intracellular esterase activity to yield the polar molecule Fluo-3, which is thus trapped within the cell. The neutrophils were then suspended in buffer that was devoid of Ca2+, and treated as shown. In (a), 1 mM Ca2+ and 1 /tM fMet-Leu-Phe were added to the suspension, as indicated by the arrows. In (b), 1 mM EGTA and 1 pM fMet-Leu-Phe were added as shown. Thus, in (a), the change in intracellular Ca2+ is due to mobilisation of intracellular Ca2+ stores and the influx of extracellular Ca2+, whereas in (b), the Ca2+ rise is due solely to release of Ca2+ from intracellular stores. Figure 6.11. Intracellular Ca2+ levels during neutrophil activation with fMet-Leu-Phe. Neutrophil suspensions were loaded with Fluo-3 AM for 15 min. This molecule is membrane permeable but cleaved by intracellular esterase activity to yield the polar molecule Fluo-3, which is thus trapped within the cell. The neutrophils were then suspended in buffer that was devoid of Ca2+, and treated as shown. In (a), 1 mM Ca2+ and 1 /tM fMet-Leu-Phe were added to the suspension, as indicated by the arrows. In (b), 1 mM EGTA and 1 pM fMet-Leu-Phe were added as shown. Thus, in (a), the change in intracellular Ca2+ is due to mobilisation of intracellular Ca2+ stores and the influx of extracellular Ca2+, whereas in (b), the Ca2+ rise is due solely to release of Ca2+ from intracellular stores.
See other pages where Neutrophil extracellular traps is mentioned: [Pg.1228]    [Pg.209]    [Pg.15]    [Pg.20]    [Pg.160]    [Pg.65]    [Pg.65]    [Pg.69]    [Pg.59]    [Pg.485]    [Pg.31]    [Pg.1228]    [Pg.209]    [Pg.15]    [Pg.20]    [Pg.160]    [Pg.65]    [Pg.65]    [Pg.69]    [Pg.59]    [Pg.485]    [Pg.31]    [Pg.63]    [Pg.338]   
See also in sourсe #XX -- [ Pg.208 ]



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