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Molecular Roles of Neutrophil Extracellular Traps in Immune Responses and Disease

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: 30 October 2025 | Viewed by 433

Special Issue Editor


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Guest Editor
Division of Gastroenterology and Hepatology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905, USA
Interests: liver diseases; immune cells; macrophages; neutrophils; mesenchymal stem cells

Special Issue Information

Dear Colleagues,

This Special Issue will explore the multiple roles of neutrophil extracellular traps (NETs) in health and disease, focusing on their molecular mechanisms and immunological consequences. NETs correspond to extracellular structures generated by a neutrophil-exclusive form of cell death known as NETosis, resulting in the secretion of genomic material and proteins with an anti-pathogen function. NETs are produced in response to inflammatory stimuli, including PAMPs and DAMPs, and have emerged as critical players in host defense, inflammation, autoimmunity, thrombosis, and cancer. Despite their protective roles against pathogens, dysregulated NET formation can contribute to chronic inflammation and subsequent tissue damage in various diseases. We invite original research articles and reviews that explore the signaling pathways driving NETosis, identify molecular components of NETs with functional significance, and investigate their interactions with other cell types. Contributions addressing novel therapeutic strategies targeting NETs or their downstream effects are also welcome. This Special Issue aims to advance our understanding of NETs in immunity and pathology by integrating immunology, molecular biology, and clinical research insights.

Dr. Sofía S. Jerez
Guest Editor

Manuscript Submission Information

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Keywords

  • neutrophils
  • NET
  • inflammation
  • chronic diseases
  • cell death

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Published Papers (1 paper)

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Research

13 pages, 1189 KB  
Article
Photoinduced Inhibition of Neutrophil Extracellular Traps Formation by Dichromatic Light Irradiation
by Kahramon Mamatkulov, Yersultan Arynbek, Huy Duc Le, Nina Vorobjeva and Grigory Arzumanyan
Curr. Issues Mol. Biol. 2025, 47(9), 729; https://doi.org/10.3390/cimb47090729 - 9 Sep 2025
Viewed by 244
Abstract
Neutrophils are the first line of defense of the human immune system against pathogens. Photobiomodulation, mediated by mitochondrial photoacceptors such as cytochrome c oxidase, has emerged as a method to modulate neutrophil function through targeted light exposure. Despite the extensive characterization of neutrophil [...] Read more.
Neutrophils are the first line of defense of the human immune system against pathogens. Photobiomodulation, mediated by mitochondrial photoacceptors such as cytochrome c oxidase, has emerged as a method to modulate neutrophil function through targeted light exposure. Despite the extensive characterization of neutrophil extracellular traps (NETs) formation (NETosis), the wavelength-specific modulation of neutrophil photoactivation and the involvement of redox pathways remain poorly defined. In this study, the effects of monochromatic (365 nm, 415 nm, 437 nm, and 625 nm) and dichromatic LED-light irradiation on NETs formation were systematically examined. The highest netotic responses were elicited by UV-A (365 nm) and violet-blue light (415 nm), whereas 437 nm showed the lowest induction and 625 nm stimulated a moderate netotic response. The pharmacological inhibition of NETosis induced by 365 nm and 415 nm irradiation with specific NADPH oxidase inhibitor, apocynin, and mitochondrial reactive oxygen species (mtROS) scavenger, MitoTEMPO, attenuated NETs formation by engaging both enzymatic and mitochondrial oxidative sources. Notably, mtROS played a dominant role under 415 nm stimulation in contrast to 365 nm-induced NETosis as demonstrated by higher sensitivity to MitoTEMPO. Importantly, combined simultaneous irradiation with 415 nm and 625 nm LEDs resulted in a significant suppression of NETs formation by more than 50%, highlighting a potent inhibitory synergy observed for the first time and suggesting a new approach of wavelength pairing to modulate neutrophil activation. These results were further supported by measurements of ROS production using a luminol-amplified chemiluminescence assay. Collectively, these findings delineate a wavelength- and ROS-dependent framework for light-induced neutrophil activation, with mitochondrial pathways exerting central control particularly under short-wavelength irradiation. Full article
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