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Methods of Protein Iodination
Published in Erwin Regoeczi, Iodine-Labeled Plasma Proteins, 2019
The enzyme (EC 1.11.1.7) is present in neutrophil granulocytes in quite large amounts, accounting for some 1 to 2%,104 or even 5%,105 of the cells’ dry weight. It has been implicated in the bacterial activity of leukocytes.106,107 Its antimicrobial and fungicidal activity requires the presence of a halide, and it has been suggested the enzyme oxidizes Cl” to hypochlorous acid (HOC1). Eosinophils are also rich in peroxidase but the neutrophil and eosinophil enzymes, both in man108 and in guinea pig,109 have different optical properties. The two guinea pig enzymes also differ in molecular weights.
Hematopoietic Organs and Blood
Published in George W. Casarett, Radiation Histopathology, 2019
Granulocytopenia develops somewhat later and to a somewhat lesser degree, despite the short circulating time of granulocytes, because of the lesser sensitivity of neutrophil granulocyte precursors in the marrow and the fairly large pool of relatively radioresistant fixed postmitotic differentiating neutrophil granulocytes in the bone marrow which continues to supply granulocytes to the blood until the pool has undergone maturation depletion (Figure 14).
Macrophage Heterogeneity
Published in Gloria H. Heppner, Amy M. Fulton, Macrophages and Cancer, 2019
Page S. Morahan, Alvin Volkman, Meryle Melnicoff, Walla L. Dempsey
The distribution of human neutrophil granulocytes into circulating and marginating pools was demonstrated by Athers and his colleagues in a series of kinetic studies.165,166 Thus, conventional blood samples tap the circulating granulocyte pool which is represented in the axial flow of blood, whereas the marginal granulocyte pool is poorly sampled by traditional methods. Cells in the marginal pool are slowly moving along the endothelium, and pool in regions of static flow. The ratio of the circulating to marginal granulocyte pool is said to be about 1:1 in the steady state. Data supporting the existence of a marginal monocyte pool in humans were later published by Meuret,167 who estimated that the circulating blood monocyte pool is approximately three to four times the size of the marginal blood monocyte pool. Closely corresponding data for marginal and circulating monocyte pools in the rat were presented by Volkman.125 More recently, Van Furth and Sluiter reported data estimating that the circulating and marginal monocyte pools in the mouse were in a 1:1 ratio.168 One implication of these data is that calculations of monocyte kinetics and putative influx have to take into account the marginal blood monocyte pool. Studies of monocyte depletion must likewise consider the pitfall of a marginal monocyte pool when estimating the effect of depletion protocols based on the number of circulating blood monocytes. This problem can be dealt with effectively by estimating the availability of residual blood monocytes for emigration in response to eliciting agents.56
Using blood calprotectin as a measure of blood neutrophils
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2021
Arne Åsberg, Lena Løfblad, Amela Felic, Marthe Wedø Aune, Gunhild Garmo Hov, Unn Merete Fagerli
Quantification of neutrophil granulocytes (measuring b-neutrophils) are regularly done in many clinical situations, for instance in monitoring cancer patients using cytostatic medications, where neutropenia is a real danger [1]. Such measurements are easily done with modern hematology instruments [2], at least when the cells are mature and normal. However, if bed-side monitoring of b-neutrophils is wanted, just a few assays are available [3,4], and none is designed for home use. For cancer patients in home care, or for patients in remote areas where hematology instruments are lacking, a robust, bed-side assay of b-neutrophils might be useful. In the hematology laboratory, neutrophil identification and counting is usually based on detection of electrical and optical properties of the cells, while a few instruments use digital image analysis [2]. We explored a chemical method of quantifying b-neutrophils, using an immunoassay to measure the concentration of calprotectin in whole blood (b-calprotectin) [5]. This principle could be applicable to a lateral flow format [6] for bed-side testing. In healthy individuals, we previously demonstrated a firm correlation between b-neutrophils and a measure of calprotectin in neutrophils, i.e. b-calprotectin adjusted for the calprotectin concentration in plasma (p-calprotectin) [5].
Prophylaxis of chemotherapy-induced neutropenia and febrile neutropenia with lipegfilgrastim in 2489 cancer patients: final results from the non-interventional study NADIR
Published in Current Medical Research and Opinion, 2019
Thomas Fietz, Andreas Lück, Holger Schulz, Johanna Harde, Christoph Losem, Sina Grebhardt, Thomas Wolff, Karin Potthoff, Udo Müller, Matthias Zaiss, Christian Martin Kurbacher
Chemotherapy-induced neutropenia and febrile neutropenia (FN) are the most common dose-limiting toxicities of myelosuppressive chemotherapy regimens1. In the case of neutropenia, a decrease in neutrophil granulocytes in the peripheral blood may result in various complications, including potential life-threatening or even fatal infections. Upon occurrence of these complications, dose reductions or cycle delays are often unavoidable, which may impact the response to the chemotherapeutic treatment2. Additionally, measures to control infections such as use of broad-spectrum antibiotics and hospitalization substantially increase the cost of therapy1,3. Depending on the number and type of comorbidities, chemotherapy-induced FN is considered to be responsible for the deaths of up to 50% of patients affected4.
Editorial – NETs in autoimmune diseases
Published in Autoimmunity, 2018
Sebastian Boeltz, Martin Herrmann
Originally, neutrophil granulocytes were described to phagocytose and kill bacteria. In 2004, a second mechanism in which neutrophils trap bacteria with extracellular DNA (NETs) was described by Brinkmann et al. [1]. They reported that microbial agents can be ensnared in decondensed chromatin released together with granule proteins. NETs are not just binding the foe [1], but also degrade virulence factors with NET-borne active enzymes [2]. Since then, a plethora of articles emerged linking NETs to host defense but also to a number of diseases – often in ambivalent roles. Literature of NET formation can be confusing as evidence often suggests both, pathognomonic or protective roles of NETs. It cannot be ignored that NETs may play a pivotal role in inflammatory diseases. This editorial summarizes a collection of articles investigating the role of NETs in autoimmune diseases.