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Neutrophil: Regulation of Functional Activation and Survival
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Neutrophil: Regulation of Functional Activation and Survival

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

Deadline for manuscript submissions: closed (31 January 2018) | Viewed by 4045

Special Issue Editor

Prof. Dr. Seiichi Kitagawa

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Guest Editor
Department of Physiology, Osaka City University, Graduate School of Medicine, Osaka, Japan
Interests: regulation of neutrophil functions; survival/apoptosis; inflamamtory cytokines; signal transduction; superoxide production; cytokine production; Toll-like receptors; migration; calpain

Special Issue Information

Dear Colleagues,

Neutrophils play a critical role, not only in the host-defense against invading microorganisms, but also in the tissue injury associated with inflammatory disorders. Neutrophils are rapidly activated by various inflammatory mediators, which include chemotactic factors, chemokines, inflammatory cytokines (such as granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, interferons, and tumor necrosis factor-a) and Toll-like receptor agonists. Neutrophil survival and apoptosis are also affected by these mediators. Activation of neutrophil functions (such as migration, phagocytosis, and superoxide and cytokine production) and neutrophil survival/apoptosis induced by inflammatory mediators are closely associated with the outcome of inflammatory disorders. Recent studies have improved our understanding about the regulatory mechanisms of neutrophil functions and survival/apoptosis at the molecular levels, and further understanding is essential to establish proper treatment of neutrophil-mediated tissue injury. It is expected that this Special Issue may cover recent advances in the regulatory mechanisms of neutrophil functions and survival/apoptosis, which may include the mediator-specific signaling pathways (such as mitogen-activated protein kinases, phosphatidylinositol 3-kinase, and Janus kinases).

Prof. Dr. Seiichi Kitagawa
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 submissions that pass pre-check are 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

  • neutrophil functions
  • inflammatory cytokines
  • signaling pathway
  • survival/apoptosis
  • Toll-like receptors
  • migration
  • mitogen-activated protein kinases
  • chemotactic factors
  • calpain

Published Papers (1 paper)

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Research

15 pages, 2281 KiB  
Article
Loss of BID Delays FASL-Induced Cell Death of Mouse Neutrophils and Aggravates DSS-Induced Weight Loss
by Simone Wicki, Ursina Gurzeler, Nadia Corazza, Vera Genitsch, Wendy Wei-Lynn Wong and Thomas Kaufmann
Int. J. Mol. Sci. 2018, 19(3), 684; https://doi.org/10.3390/ijms19030684 - 28 Feb 2018
Cited by 6 | Viewed by 3755
Abstract
Neutrophils are key players in the early defense against invading pathogens. Due to their potent effector functions, programmed cell death of activated neutrophils has to be tightly controlled; however, its underlying mechanisms remain unclear. Fas ligand (FASL/CD95L) has been shown to induce neutrophil [...] Read more.
Neutrophils are key players in the early defense against invading pathogens. Due to their potent effector functions, programmed cell death of activated neutrophils has to be tightly controlled; however, its underlying mechanisms remain unclear. Fas ligand (FASL/CD95L) has been shown to induce neutrophil apoptosis, which is accelerated by the processing of the BH3-only protein BH3 interacting domain death agonist (BID) to trigger mitochondrial apoptotic events, and been attributed a regulatory role during viral and bacterial infections. Here, we show that, in accordance with previous works, mouse neutrophils underwent caspase-dependent apoptosis in response to FASL, and that this cell death was significantly delayed upon loss of BID. However, pan-caspase inhibition failed to protect mouse neutrophils from FASL-induced apoptosis and caused a switch to RIPK3-dependent necroptotic cell death. Intriguingly, such a switch was less evident in the absence of BID, particularly under inflammatory conditions. Delayed neutrophil apoptosis has been implicated in several auto-inflammatory diseases, including inflammatory bowel disease. We show that neutrophil and macrophage driven acute dextran sulfate sodium (DSS) induced colitis was slightly more aggravated in BID-deficient mice, based on significantly increased weight loss compared to wild-type controls. Taken together, our data support a central role for FASL > FAS and BID in mouse neutrophil cell death and further underline the anti-inflammatory role of BID. Full article
(This article belongs to the Special Issue Neutrophil: Regulation of Functional Activation and Survival)
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