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Special Issue "Neutrophils in Chronic Inflammation"

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: 31 January 2022.

Special Issue Editor

Dr. Christian D. Sadik
E-Mail Website
Guest Editor
Department of Dermatology, Universität zu Lübeck, Lübeck, Germany
Interests: innate immunity; granulocytes; autoimmune diseases; skin inflammation; lipid mediators; Fc gamma receptors

Special Issue Information

Dear Colleagues,

Neutrophils were traditionally considered to be mere effector cells primarily involved in acute inflammation in response to bacterial and fungal infections. In recent years, it has been increasingly appreciated that neutrophils also play a major role in sterile, chronic inflammation, including in autoimmune and autoinflammatory diseases, metabolic disease, and cancers. Furthermore, it has become evident that in addition to their role as final effector cells, neutrophils also exert important regulatory functions throughout the entire course of tissue inflammation, from its emergence to its resolution. Together, several lines of evidence now also suggest that neutrophils are phenotypically heterogenous; thus, the neutrophil population constitutes a large spectrum of phenotypes or may be even composed of different subpopulations. In this Special Issue “Neutrophils in Chronic Inflammation”, we therefore compile studies further elucidating the regulatory function of neutrophils in sterile inflammation as well as the molecular pathways regulating neutrophil activity in sterile tissue inflammation. Many of these molecular pathways are themselves neutrophil-derived, thus leading to a regulation of neutrophils by neutrophils. In that context, we are also looking for manuscripts providing novel findings on the heterogeneity of neutrophil populations.

Dr. Christian D. Sadik 
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neutrophils
  • sterile inflammation
  • neutrophil heterogeneity
  • regulatory functions of neutrophils

Published Papers (2 papers)

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Research

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Article
LPS Induces Opposing Memory-like Inflammatory Responses in Mouse Bone Marrow Neutrophils
Int. J. Mol. Sci. 2021, 22(18), 9803; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22189803 - 10 Sep 2021
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Abstract
A growing body of evidence suggests that innate immune cells can respond in a memory-like (adaptive) fashion, which is referred to as trained immunity. Only few in vivo studies have shown training effects in neutrophils; however, no in vitro setup has been established [...] Read more.
A growing body of evidence suggests that innate immune cells can respond in a memory-like (adaptive) fashion, which is referred to as trained immunity. Only few in vivo studies have shown training effects in neutrophils; however, no in vitro setup has been established to study the induction of trained immunity or tolerance in neutrophils by microbial agents. In light of their short lifespan (up to 48 h), we suggest to use the term trained sensitivity for neutrophils in an in vitro setting. Here, we firstly describe a feasible two-hit model, using different doses of lipopolysaccharide (LPS) in bone marrow neutrophils. We found that low doses (10 pg/mL) induce pro-inflammatory activation (trained sensitivity), whereas priming with high doses (100 ng/mL) leads to suppression of pro-inflammatory mediators such as TNF-α or IL-6 (tolerance) (p < 0.05). On a functional level, trained neutrophils displayed increased phagocytic activity and LFA-1 expression as well as migrational capacity and CD11a expression, whereas tolerant neutrophils show contrasting effects in vitro. Mechanistically, TLR4/MyD88/PI3Ks regulate the activation of p65, which controls memory-like responses in mouse bone marrow neutrophils (p < 0.05). Our results open a new window for further in vitro studies on memory-like inflammatory responses of short-lived innate immune cells such as neutrophils. Full article
(This article belongs to the Special Issue Neutrophils in Chronic Inflammation)
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Review

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Review
The Role of Neutrophilic Granulocytes in Philadelphia Chromosome Negative Myeloproliferative Neoplasms
Int. J. Mol. Sci. 2021, 22(17), 9555; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179555 - 03 Sep 2021
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Abstract
Philadelphia chromosome negative myeloproliferative neoplasms (MPN) are composed of polycythemia vera (PV), essential thrombocytosis (ET), and primary myelofibrosis (PMF). The clinical picture is determined by constitutional symptoms and complications, including arterial and venous thromboembolic or hemorrhagic events. MPNs are characterized by mutations in [...] Read more.
Philadelphia chromosome negative myeloproliferative neoplasms (MPN) are composed of polycythemia vera (PV), essential thrombocytosis (ET), and primary myelofibrosis (PMF). The clinical picture is determined by constitutional symptoms and complications, including arterial and venous thromboembolic or hemorrhagic events. MPNs are characterized by mutations in JAK2, MPL, or CALR, with additional mutations leading to an expansion of myeloid cell lineages and, in PMF, to marrow fibrosis and cytopenias. Chronic inflammation impacting the initiation and expansion of disease in a major way has been described. Neutrophilic granulocytes play a major role in the pathogenesis of thromboembolic events via the secretion of inflammatory markers, as well as via interaction with thrombocytes and the endothelium. In this review, we discuss the molecular biology underlying myeloproliferative neoplasms and point out the central role of leukocytosis and, specifically, neutrophilic granulocytes in this group of disorders. Full article
(This article belongs to the Special Issue Neutrophils in Chronic Inflammation)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title 1: The association of neutrophil related inflammatory markers in post stroke dementia

Y.-Y.Wu, Y.-L.L., W.-M.H., and Y.-C.Chen

Abstract: Inflammatory mechanism played a role in stroke patients, from acute stroke stage to post stroke chronic stage. Elevated neutrophil had been observed in post stroke late phase, which may have interaction with cytokines that determinate post stroke dementia. We enrolled 128 patients with chronic stroke and age-, sex- matched controls. While lower levels of EGF, GRO, sCD40L, and IL-7 were noted in patients with post-stroke dementia, compared to those without dementia, there was no difference in the level of IL-17A, and IL-4. In comparison between dementia and non-dementia of post stroke patients, the level of IL-4 was higher in post stroke dementia. Neutrophil related inflammatory markers had strong association with both post stroke late phase patient and post stroke dementia.

Previous studies showed elevated neutrophil in post stroke phase. We examined the neutrophil related inflammatory marker and validated the importance of neutrophil in those with post-stroke dementia. To our knowledge, this is the first report of neutrophil related inflammatory marker in post stroke late phase in Asian subjects.

We checked inflammatory markers in post stroke late phase, which had been reported having relationship with neutrophil in previous studies. GRO contributes to neutrophil chemotaxis in chronic inflammatory. CD40-CD40L-mediated processes in oxidative stress, inflammatory pathways and vascular diseases. In vascular inflammation, CD40-CD40L interactions induce activation of p38 MAPK, and further drives neutrophil activation. Epidermal growth factor (EFG) regulates expression of neutrophil and alleviates cerebral ischemia-induced brain injury. IL-4 is a potent activator of de novo protein synthesis in neutrophils and activates neutrophil cytoskeletal rearrangements. IL-17 exerted pro-inflammatory effect to promote neutrophil-mediated immunity. In mouse model, IL-17 regulated immune response including neutrophil infiltration, natural killer T cells (NKT) activation, IFNg production, and ultimately inflammation. IL-7 initiates a T-cell receptor-independent (TCR-independent) expansion of NKT17 cells, thus supporting IL-17 homeostasis. Although less relationship with neutrophil, IL-7 influences neural development at a molecular level by participating in human brain architecture through glia cell formation and has a physiological role in human organ development and progenitor cell differentiation.
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