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Neutrophil Extracellular Traps (NETs) in Human Disease: From Molecular Mechanisms...
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Neutrophil Extracellular Traps (NETs) in Human Disease: From Molecular Mechanisms to Therapeutic Translation

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 September 2026 | Viewed by 428

Special Issue Editors

Prof. Dr. Michael Boettcher

E-Mail Website
Guest Editor
1. Department of Pediatric Surgery, University Medical Center Mannheim, Heidelberg University, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany
2. Department of Pediatric Surgery, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany
Interests: immunomodulation; neutrophil extracellular traps; NETs; CAR t-cells; pediatric tumor
Special Issues, Collections and Topics in MDPI journals
Dr. Julia Elrod

E-Mail Website
Guest Editor
Universitätsklinikum Mannheim, Mannheim, Germany
Interests: neutrophil extracellular traps

Special Issue Information

Dear Colleagues,

This Special Issue invites original research papers and reviews on the molecular machinery of neutrophil extracellular traps (NETs) in the context of human disease. We also welcome studies at the interface of surgery and oncology, including perioperative NET induction, ischemia–reperfusion and biomaterial/implant interactions, wound and anastomotic healing, adhesion formation, immunothrombosis, and postoperative complications. In oncology, we seek mechanistic work on how NETs shape the tumor microenvironment, capture circulating tumor cells, promote metastasis, modulate responses to chemo-/radiotherapy and immunotherapy, and affect outcomes after oncologic surgery. Beyond oncology, submissions on infection and sepsis, cardio-/cerebrovascular disease, pulmonary injury/ARDS, autoimmunity, metabolic disease, renal/hepatic injury, neuroinflammation, and maternal–fetal medicine are encouraged. Translational contributions on diagnostics and biomarkers, device/implant surface engineering, and therapeutic strategies, including preclinical and clinical studies, are especially welcome.

Prof. Dr. Michael Boettcher
Dr. Julia Elrod
Guest Editors

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 250 words) can be sent to the Editorial Office for assessment.

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 extracellular traps (NETs)
  • molecular mechanisms
  • human disease

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Published Papers (1 paper)

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Research

15 pages, 2112 KB  
Article
Intraperitoneal G-CSF Stimulation Achieves Human-like Neutrophil Levels in NSG Mice Without Inducing Systemic Inflammation
by Richard Elrod, Yuqing Lu, Christoph Brochhausen, Rebecca Schönmehl, Martin Herrmann, Hong Zhang, Christoph Mohr, Yannick Ledermann, Laura Blum, Michael Boettcher, Michaela Klinke-Petrowsky, Jasmin Knopf and Julia Elrod
Int. J. Mol. Sci. 2026, 27(11), 5099; https://doi.org/10.3390/ijms27115099 - 4 Jun 2026
Viewed by 73
Abstract
Neutrophils are central executors of innate immunity. Yet murine models are inherently limited by low baseline neutrophil counts. NSG mice are among the most widely used models for xenotransplantation and studies on the humanized immune system. Although G-CSF is known to stimulate granulopoiesis, [...] Read more.
Neutrophils are central executors of innate immunity. Yet murine models are inherently limited by low baseline neutrophil counts. NSG mice are among the most widely used models for xenotransplantation and studies on the humanized immune system. Although G-CSF is known to stimulate granulopoiesis, the dose- and schedule-dependent effects of intraperitoneal G-CSF administration have not been systematically characterized in this immunodeficient background. Male NSG mice received intraperitoneal G-CSF according to one of five regimens (n = 6 per group): group 0 served as the saline control, group 1 received a single dose of 250 µg/kg G-CSF administered at 48 h; group 2 received a single dose of 250 µg/kg G-CSF administered at 24 h; group 3 received three doses of 250 µg/kg administered G-CSF at 0 h, 24 h, and 48 h and group 4 received a single dose of 500 µg/kg G-CSF administered at 48 h. All animals were sacrificed at 72 h. Circulating neutrophils were then quantified by flow cytometry, bone marrow neutrophil proportions by panoptic smear analysis, and splenic neutrophil abundance by Ly6G immunofluorescence. Systemic neutrophil activation was assessed via plasma neutrophil elastase (NE) activity and cell-free DNA (cfDNA) levels. Repeated G-CSF administration (Group 3) induced an approximately 13-fold expansion of circulating neutrophils, approaching the human physiological range, with significant increases also observed in bone marrow and a trend towards increased neutrophil abundance in the spleen. A single dose of 250 µg/kg administered at 24 h (group 2), produced significant neutrophil expansion in peripheral blood and bone marrow but not in the spleen, while all other single-dose regimens failed to induce significant expansion in any compartment. NE activity and cfDNA concentrations and a selected cytokine panel remained unaltered across all groups. This systematic comparison establishes repeated intraperitoneal G-CSF administration as a reproducible strategy to achieve human-like neutrophil levels in NSG mice without inducing systemic inflammation. This provides a validated protocol with direct utility in translational models of neutrophil-dependent diseases. Full article
(This article belongs to the Special Issue Neutrophil Extracellular Traps (NETs) in Human Disease: From Molecular Mechanisms to Therapeutic Translation)
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