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The Research of Neutrophil

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 18722

Special Issue Editor

Dept Lab Diagnost & Clin Immunol Dev Age, Medical University of Warsaw, Warsaw, Poland
Interests: immunology; inflammation; tumor development; autoimmunity; neutrophil extracellular traps
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neutrophils are the most abundant, short-lived, and terminally differentiated white blood cells. They constitute the first line of defense against foreign invaders using major effector mechanisms: phagocytosis, degranulation, and NETs formation. Traditionally neutrophils were considered as terminally differentiated, homogenous cell populations of the innate immune response, however, different studies started to highlight the subpopulation heterogeneity and pivotal role in immunity,  inflammation and cancer. All scientists involved in the field of neutrophil biology are welcome to contribute to the understanding of the role of neutrophil in physiology and pathology, providing clues for better management and newer therapeutic opportunities for neutrophil-centric disorders. Both original and review papers are welcome.

Prof. Urszula Demkow
Guest Editor

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Keywords

  • neutrophil
  • neutrophil extracellular traps
  • neutrophils in the pathogenesis of inflammatory diseases
  • neutrophils in tumor development
  • neutrophil cooperation with other immune cells
  • neutrophil and autoimmunity

Published Papers (5 papers)

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Research

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27 pages, 9763 KiB  
Article
Depletion of Lipocalin 2 (LCN2) in Mice Leads to Dysbiosis and Persistent Colonization with Segmented Filamentous Bacteria
by Patrick Klüber, Steffen K. Meurer, Jessica Lambertz, Roman Schwarz, Silke Zechel-Gran, Till Braunschweig, Sabine Hurka, Eugen Domann and Ralf Weiskirchen
Int. J. Mol. Sci. 2021, 22(23), 13156; https://doi.org/10.3390/ijms222313156 - 05 Dec 2021
Cited by 17 | Viewed by 3853
Abstract
Lipocalin 2 (LCN2) mediates key roles in innate immune responses. It has affinity for many lipophilic ligands and binds various siderophores, thereby limiting bacterial growth by iron sequestration. Furthermore, LCN2 protects against obesity and metabolic syndrome by interfering with the composition of gut [...] Read more.
Lipocalin 2 (LCN2) mediates key roles in innate immune responses. It has affinity for many lipophilic ligands and binds various siderophores, thereby limiting bacterial growth by iron sequestration. Furthermore, LCN2 protects against obesity and metabolic syndrome by interfering with the composition of gut microbiota. Consequently, complete or hepatocyte-specific ablation of the Lcn2 gene is associated with higher susceptibility to bacterial infections. In the present study, we comparatively profiled microbiota in fecal samples of wild type and Lcn2 null mice and show, in contrast to previous reports, that the quantity of DNA in feces of Lcn2 null mice is significantly lower than that in wild type mice (p < 0.001). By using the hypervariable V4 region of the 16S rDNA gene and Next-Generation Sequencing methods, we found a statistically significant change in 16 taxonomic units in Lcn2-/- mice, including eight gender-specific deviations. In particular, members of Clostridium, Escherichia, Helicobacter, Lactococcus, Prevotellaceae_UCG-001 and Staphylococcus appeared to expand in the intestinal tract of knockout mice. Interestingly, the proportion of Escherichia (200-fold) and Staphylococcus (10-fold) as well as the abundance of intestinal bacteria encoding the LCN2-sensitive siderphore enterobactin (entA) was significantly increased in male Lcn2 null mice (743-fold, p < 0.001). This was accompanied by significant higher immune cell infiltration in the ileum as demonstrated by increased immunoreactivity against the pan-leukocyte protein CD45, the lymphocyte transcription factor MUM-1/IRF4, and the macrophage antigen CD68/Macrosialin. In addition, we found a higher expression of mucosal mast cell proteases indicating a higher number of those innate immune cells. Finally, the ileum of Lcn2 null mice displayed a high abundance of segmented filamentous bacteria, which are intimately associated with the mucosal cell layer, provoking epithelial antimicrobial responses and affecting T-helper cell polarization. Full article
(This article belongs to the Special Issue The Research of Neutrophil)
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Review

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16 pages, 795 KiB  
Review
Molecular Mechanisms of Neutrophil Extracellular Trap (NETs) Degradation
by Urszula Demkow
Int. J. Mol. Sci. 2023, 24(5), 4896; https://doi.org/10.3390/ijms24054896 - 03 Mar 2023
Cited by 15 | Viewed by 4343
Abstract
Although many studies have been exploring the mechanisms driving NETs formation, much less attention has been paid to the degradation and elimination of these structures. The NETs clearance and the effective removal of extracellular DNA, enzymatic proteins (neutrophil elastase, proteinase 3, myeloperoxidase) or [...] Read more.
Although many studies have been exploring the mechanisms driving NETs formation, much less attention has been paid to the degradation and elimination of these structures. The NETs clearance and the effective removal of extracellular DNA, enzymatic proteins (neutrophil elastase, proteinase 3, myeloperoxidase) or histones are necessary to maintain tissue homeostasis, to prevent inflammation and to avoid the presentation of self-antigens. The persistence and overabundance of DNA fibers in the circulation and tissues may have dramatic consequences for a host leading to the development of various systemic and local damage. NETs are cleaved by a concerted action of extracellular and secreted deoxyribonucleases (DNases) followed by intracellular degradation by macrophages. NETs accumulation depends on the ability of DNase I and DNAse II to hydrolyze DNA. Furthermore, the macrophages actively engulf NETs and this event is facilitated by the preprocessing of NETs by DNase I. The purpose of this review is to present and discuss the current knowledge about the mechanisms of NETs degradation and its role in the pathogenesis of thrombosis, autoimmune diseases, cancer and severe infections, as well as to discuss the possibilities for potential therapeutic interventions. Several anti-NETs approaches had therapeutic effects in animal models of cancer and autoimmune diseases; nevertheless, the development of new drugs for patients needs further study for an effective development of clinical compounds that are able to target NETs. Full article
(This article belongs to the Special Issue The Research of Neutrophil)
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18 pages, 570 KiB  
Review
The Impact of Cytokines on Neutrophils’ Phagocytosis and NET Formation during Sepsis—A Review
by Barbara Gierlikowska, Albert Stachura, Wojciech Gierlikowski and Urszula Demkow
Int. J. Mol. Sci. 2022, 23(9), 5076; https://doi.org/10.3390/ijms23095076 - 03 May 2022
Cited by 5 | Viewed by 3306
Abstract
Sepsis is an overwhelming inflammatory response to infection, resulting in multiple-organ injury. Neutrophils are crucial immune cells involved in innate response to pathogens and their migration and effector functions, such as phagocytosis and neutrophil extracellular trap (NET) formation, are dependent on cytokine presence [...] Read more.
Sepsis is an overwhelming inflammatory response to infection, resulting in multiple-organ injury. Neutrophils are crucial immune cells involved in innate response to pathogens and their migration and effector functions, such as phagocytosis and neutrophil extracellular trap (NET) formation, are dependent on cytokine presence and their concentration. In the course of sepsis, recruitment and migration of neutrophils to infectious foci gradually becomes impaired, thus leading to loss of a crucial arm of the innate immune response to infection. Our review briefly describes the sepsis course, the importance of neutrophils during sepsis, and explains dependence between cytokines and their activation. Moreover, we, for the first time, summarize the impact of cytokines on phagocytosis and NET formation. We highlight and discuss the importance of cytokines in modulation of both processes and emphasize the direction of further investigations. Full article
(This article belongs to the Special Issue The Research of Neutrophil)
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23 pages, 1296 KiB  
Review
Neutrophil Death in Myeloproliferative Neoplasms: Shedding More Light on Neutrophils as a Pathogenic Link to Chronic Inflammation
by Dragana Marković, Irina Maslovarić, Dragoslava Djikić and Vladan P. Čokić
Int. J. Mol. Sci. 2022, 23(3), 1490; https://doi.org/10.3390/ijms23031490 - 27 Jan 2022
Cited by 7 | Viewed by 3642
Abstract
Neutrophils are an essential component of the innate immune response, but their prolonged activation can lead to chronic inflammation. Consequently, neutrophil homeostasis is tightly regulated through balance between granulopoiesis and clearance of dying cells. The bone marrow is both a site of neutrophil [...] Read more.
Neutrophils are an essential component of the innate immune response, but their prolonged activation can lead to chronic inflammation. Consequently, neutrophil homeostasis is tightly regulated through balance between granulopoiesis and clearance of dying cells. The bone marrow is both a site of neutrophil production and the place they return to and die. Myeloproliferative neoplasms (MPN) are clonal hematopoietic disorders characterized by the mutations in three types of molecular markers, with emphasis on Janus kinase 2 gene mutation (JAK2V617F). The MPN bone marrow stem cell niche is a site of chronic inflammation, with commonly increased cells of myeloid lineage, including neutrophils. The MPN neutrophils are characterized by the upregulation of JAK target genes. Additionally, MPN neutrophils display malignant nature, they are in a state of activation, and with deregulated apoptotic machinery. In other words, neutrophils deserve to be placed in the midst of major events in MPN. Our crucial interest in this review is better understanding of how neutrophils die in MPN mirrored by defects in apoptosis and to what possible extent they can contribute to MPN pathophysiology. We tend to expect that reduced neutrophil apoptosis will establish a pathogenic link to chronic inflammation in MPN. Full article
(This article belongs to the Special Issue The Research of Neutrophil)
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11 pages, 809 KiB  
Review
The Role of Neutrophils in the Pathogenesis of Chronic Lymphocytic Leukemia
by Malgorzata Wachowska, Alicja Wojciechowska and Angelika Muchowicz
Int. J. Mol. Sci. 2022, 23(1), 365; https://doi.org/10.3390/ijms23010365 - 29 Dec 2021
Cited by 4 | Viewed by 2379
Abstract
Tumor-associated neutrophils appear to be a crucial element of the tumor microenvironment that actively participates in the development and progression of cancerous diseases. The increased lifespan, plasticity in changing of phenotype, and functions of neutrophils influence the course of the disease and may [...] Read more.
Tumor-associated neutrophils appear to be a crucial element of the tumor microenvironment that actively participates in the development and progression of cancerous diseases. The increased lifespan, plasticity in changing of phenotype, and functions of neutrophils influence the course of the disease and may significantly affect survival. In patients with chronic lymphocytic leukemia (CLL), disturbances in neutrophils functions impede the effective immune defense against pathogens. Therefore, understanding the mechanism underlying such a phenomenon in CLL seems to be of great importance. Here we discuss the recent reports analyzing the phenotype and functions of neutrophils in CLL, the most common leukemia in adults. We summarize the data concerning both the phenotype and the mechanisms by which neutrophils directly support the proliferation and survival of malignant B cells. Full article
(This article belongs to the Special Issue The Research of Neutrophil)
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