Life of neutrophil: From stem cell to neutrophil extracellular trap

Olmesartan Prevented Intra-articular Inflammation Induced by Zymosan in Rats

“…Recently, some authors have suggested that the formation of neutrophil extracellular traps (NETs) has the advantage of cancelling large bio-structures, such that fungi cannot be internalised by phagocytes. 29) NETs participate in the pathogenesis of autoimmune diseases; in patients with RA, NET formation stimulates synovial fibroblasts to produce pro-inflammatory mediators that participate in joint injury. 30) In this study and in other experimental models of inflammation, OLM reduced the expression of COX-2, which could result in tissue protection.…”

Foreword

“…They highlight the easiest and highly cost effective preventive measure of antiflu vaccinations, still underestimated and at ashamedly low rate, but holding the greatest potential to tame the infection. Arazna et al (2013) and Pruchniak et al (2013) review the current knowledge on a rapidly evolving area of research devoted to the innate immunity carried by neutrophils, consisting of their ability to form extracellular traps (NETs) in response to pathogen invasion. The nuclear DNA is usually used to build a trap, and neutrophils die in the process.…”

NTangled

“…In this wild world were born neutrophils (NTs), the innate immune system's ingenious killing machines on rampage [8]. Lingering in the blood stream, the bone marrow and organs, principally the pulmonary vascular bed [9], neutrophils turn up almost immediately at the sites of infection, crawling through endothelial barriers and tissues [10,11].…”

“…The risks and undesired effects of ex vivo cell cultures when it comes to the immune system were addressed in a previous highlight [18]. Of course, the short life of neutrophils compromises the establishment of cell lines [14] and their resistance to molecular manipulation renders studies complicated to design and decode [8], moreover the reactions of murine neutrophils differ from their human counterpart, at least ex vivo [12]. The gap between the natural hunting ground of neutrophils, a highly complex 3D architecture of tissues, liquids and interlocutors and a culture dish is as enormous as impossible to bridge by simulation.…”

“…The gap between the natural hunting ground of neutrophils, a highly complex 3D architecture of tissues, liquids and interlocutors and a culture dish is as enormous as impossible to bridge by simulation. Neutrophil homeostasis between a stem cell, progenitor and post-mitotic pool is extremely fine-tuned [8,11] and subjected to circadian fluctuations depending on light and the sympathetic nervous system [9] plus a constant bidirectional dialog with other members of the immune system, namely dendritic cells, macrophages and T cells [8,16]. In consideration of the urgent nature of fighting a microbial invasion and the hypothesis that NETs are meant to prevent invaders from spreading [10], in particular the tardiness of NET release ex vivo e ranging from 1 to 4 h depending on the study e is suspicious [12,16].…”