Journal Browser

Journal Browser

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 "Biochemistry".

Deadline for manuscript submissions: 31 May 2021.

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; Fcgamma 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.


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

Published Papers

This special issue is now open for submission, see below for planned papers.

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.
Back to TopTop