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Mari van de Vyver

inflammatory process is well described in literature and consists of two sequential phases, the first involving neutrophil, monocyte/macrophage recruitment, and activation as illustrated in Fig. 3A . In the absence of infection, the primary aim of this initial

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Da-Long Ren, Ai-Ai Sun, Ya-Juan Li, Min Chen, Shu-Chao Ge, and Bing Hu

regulating role in neutrophil migration ( Ren et al . 2015 ), and this finding motivated us to further explore the potential effect of exogenous melatonin on neutrophil function. Thus, this study aimed to investigate, in vivo , the effect of exogenous

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Ling-Chu Chang, Sally A Madsen, Trine Toelboell, Patty S D Weber, and Jeanne L Burton

Introduction Neutrophils are one of the most important immune cells regulating acute inflammation after trauma and infection. The best-known function of neutrophils is their bactericidal activity, which is accomplished by release of

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T C Alba-Loureiro, S M Hirabara, J R Mendonça, R Curi, and T C Pithon-Curi

Introduction Patients with diabetes mellitus have increased susceptibility to and severity of infections. Several studies have shown alterations in neutrophil function, an effect that contributes to the high incidence of infections

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Eddy Himpe, Céline Degaillier, Astrid Coppens, and Ron Kooijman

Introduction Neutrophils are pivotal effector cells in the innate immune response. They are phagocytic cells that participate in inflammatory reactions as a first line of defense against invading micro-organisms. Neutrophils are recruited to sites

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Gonzalo Alba, Consuelo Santa-María, María Edith Reyes-Quiroz, Rajaa El Bekay, Isabel Geniz, José Martín-Nieto, Elizabeth Pintado, and Francisco Sobrino

the CN active site ( Namgaladze et al . 2002 ). Although CN function is particularly important in brain, cartilage, and lymphocytes, we have shown that neutrophils also exhibit high CN expression ( Carballo et al . 1999 ). Neutrophils, in addition to

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Katie J Mylonas, Neil A Turner, Sumia A Bageghni, Christopher J Kenyon, Christopher I White, Kieran McGregor, Robert A Kimmitt, Richard Sulston, Valerie Kelly, Brian R Walker, Karen E Porter, Karen E Chapman, and Gillian A Gray

Introduction Ischemic cell death associated with myocardial infarction (MI) prompts the recruitment and activation of immune cells to ensure repair ( Epelman & Mann 2012 , Frangogiannis 2012 ). Neutrophils are recruited early, removing

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Lesley A Hill, Dimitra A Vassiliadi, Ioanna Dimopoulou, Anna J Anderson, Luke D Boyle, Alixe H M Kilgour, Roland H Stimson, Yoan Machado, Christopher M Overall, Brian R Walker, John G Lewis, and Geoffrey L Hammond

(RCL) that is characteristic of the SERPIN structure ( Gettins & Olson 2016 ). While CBG is not known to inhibit proteases, its RCL is cleaved by neutrophil elastase (NE) ( Hammond et al. 1990 ), chymotrypsin ( Lewis & Elder 2014 ) and Pseudomonas

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Shiyun Tong, Shumin Yang, Ting Li, Rufei Gao, Jinbo Hu, Ting Luo, Hua Qing, Qianna Zhen, Renzhi Hu, Xuan Li, Yi Yang, Chuan Peng, and Qifu Li

increasing concentrations of plasma BPA ( Krieter et al. 2013 ). However, the mechanism of pathology has not been thoroughly elucidated to date. Neutrophil extracellular traps (NETs), which is also known as NETosis, is a DNA skeleton coated with cytosolic

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M De la Fuente, M Carrasco, and A Hernanz


We have studied the effects in vitro of gastrin-17 and gastrin-34, at concentrations from 10−14 m to 10−6 m, on several of the functions of peripheral blood human neutrophils, i.e. adherence to substrate, mobility (spontaneous and directed by a chemical gradient or chemotaxis), ingestion of inert particles (latex beads) and cells (Candida albicans) and superoxide anion production. Both gastrins inhibited several steps of the phagocytic process of human neutrophils, such as mobility and ingestion. By contrast, these peptides increased adherence and had no effect on superoxide anion production. In general, these effects were significant at peptide concentrations between 10−12 m and 10−8 m with a maximal effect at 10−10 m. In addition, gastrin peptides induced a significant increase in intracellular cAMP levels at 30, 60 and 120 s. Moreover, the inhibitory effect of gastrin-17 on the ingestion capacity of neutrophils (latex bead phagocytosis) was similar to that obtained with EGTA, a well-known extracellular calcium chelating compound. Gastrin-17 was found to inhibit completely the stimulation of latex bead phagocytosis in neutrophils caused by the calcium ionophore A23187. These results suggest that gastrin is a negative modulator of the phagocytic process of human neutrophils, and that this effect might involve an increase in intracellular cAMP levels and a decrease in calcium entry into the cells.

Journal of Endocrinology (1997) 153, 475–483