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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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PG McTernan, MC Sheppard, and GR Williams

HL60 cells differentiate to monocytes or neutrophils in response to 1 alpha,25(OH)2-vitamin D3 (D3) and retinoids respectively. D3 and retinoid actions converge since their receptors (VDR, RAR) heterodimerise with a common partner, RXR, which also interacts with thyroid hormone (T3) receptors (T3R). HL60 cells were treated with combinations of D3 and retinoids to induce differentiation and to investigate whether increased VDR or RAR expression correlated with monocyte or neutrophil differentiation and whether altered receptor concentrations affected DNA-binding specificity. As assessed by Western blotting, VDR and RXR expression was unchanged in monocytes relative to controls but levels of RAR and T3R were reduced. In contrast, only VDR expression was reduced in neutrophils. T3 did not promote differentiation or influence its induction by D3 or retinoids and did not affect expression of any receptor. Gel mobility-shift analysis revealed that nuclear extracts from undifferentiated cells, monocytes and neutrophils interacted differently with VDRE-, RARE- and RXRE-binding sites. Monocyte nuclear protein/DNA complexes contain readily detectable VDR and RXR whereas neutrophil complexes contain RAR and RXR. Thus hormone-induced changes in receptor stoichiometry favour either VDR/RXR or RAR/RXR heterodimerisation and correlate with hormone-induced differentiation of HL60 cells to monocytes or neutrophils respectively.