Innovative nanoparticle-based approaches for modulating neutrophil extracellular traps in diseases: from mechanisms to therapeutics

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Abstract

Neutrophil extracellular traps (NETs) participate in both host defense and the pathogenesis of various diseases, such as infections, thrombosis, and tumors. While they help capture and eliminate pathogens, NETs’ excessive or dysregulated formation can lead to tissue damage and disease progression. Therapeutic strategies targeting NET modulation have shown potential, but challenges remain, particularly in achieving precise drug delivery and maintaining drug stability. Nanoparticle (NP)-based drug delivery systems offer innovative solutions for overcoming the limitations of conventional therapies. This review explores the biological mechanisms of NET formation, their interactions with NPs, and the therapeutic applications of NP-based drug delivery systems for modulating NETs. We discuss how NPs can be designed to either promote or inhibit NET formation and provide a comprehensive analysis of their potential in treating NET-related diseases. Additionally, we address the current challenges and future prospects for NP-based therapies in NET research, aiming to bridge the gap between nanotechnology and NET modulation for the development of novel therapeutic approaches.

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Most cited references 181

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Neutrophil extracellular traps kill bacteria.

V Brinkmann (2004)

Neutrophils engulf and kill bacteria when their antimicrobial granules fuse with the phagosome. Here, we describe that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria. These neutrophil extracellular traps (NETs) degrade virulence factors and kill bacteria. NETs are abundant in vivo in experimental dysentery and spontaneous human appendicitis, two examples of acute inflammation. NETs appear to be a form of innate response that binds microorganisms, prevents them from spreading, and ensures a high local concentration of antimicrobial agents to degrade virulence factors and kill bacteria.

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Neutrophil extracellular traps in immunity and disease

Venizelos Papayannopoulos (2017)

Neutrophils are innate immune phagocytes that have a central role in immune defence. Our understanding of the role of neutrophils in pathogen clearance, immune regulation and disease pathology has advanced dramatically in recent years. Web-like chromatin structures known as neutrophil extracellular traps (NETs) have been at the forefront of this renewed interest in neutrophil biology. The identification of molecules that modulate the release of NETs has helped to refine our view of the role of NETs in immune protection, inflammatory and autoimmune diseases and cancer. Here, I discuss the key findings and concepts that have thus far shaped the field of NET biology.

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Platelet TLR4 activates neutrophil extracellular traps to ensnare bacteria in septic blood.

Stephen R Clark, Adrienne C Ma, Samantha A Tavener … (2007)

It has been known for many years that neutrophils and platelets participate in the pathogenesis of severe sepsis, but the inter-relationship between these players is completely unknown. We report several cellular events that led to enhanced trapping of bacteria in blood vessels: platelet TLR4 detected TLR4 ligands in blood and induced platelet binding to adherent neutrophils. This led to robust neutrophil activation and formation of neutrophil extracellular traps (NETs). Plasma from severely septic humans also induced TLR4-dependent platelet-neutrophil interactions, leading to the production of NETs. The NETs retained their integrity under flow conditions and ensnared bacteria within the vasculature. The entire event occurred primarily in the liver sinusoids and pulmonary capillaries, where NETs have the greatest capacity for bacterial trapping. We propose that platelet TLR4 is a threshold switch for this new bacterial trapping mechanism in severe sepsis.

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Author and article information

Contributors

Chang Wang: wangchang@jlu.edu.cn

Tianmeng Sun: tsun41@jlu.edu.cn

Shuhan Liu: liushuhan@jlu.edu.cn

Journal

Journal ID (nlm-ta): J Nanobiotechnology

Journal ID (iso-abbrev): J Nanobiotechnology

Title: Journal of Nanobiotechnology

Publisher: BioMed Central (London )

ISSN (Electronic): 1477-3155

Publication date (Electronic): 6 February 2025

Publication date PMC-release: 6 February 2025

Publication date Collection: 2025

Volume: 23

Electronic Location Identifier: 88

Affiliations

[1 ]Cancer Center, The First Hospital, Jilin University, ( https://ror.org/00js3aw79) Changchun, Jilin China

[2 ]Key Laboratory of Organ Regeneration and Transplantation of Ministry of Education, Institute of Immunology, The First Hospital, Jilin University, ( https://ror.org/00js3aw79) Changchun, Jilin China

[3 ]Department of Neurosurgery, The First Hospital, Jilin University, ( https://ror.org/00js3aw79) Changchun, Jilin China

[4 ]Department of Hematology, The Second Clinical Medical College of Shanxi Medical University, ( https://ror.org/0265d1010) Taiyuan, Shanxi China

[5 ]National-Local Joint Engineering Laboratory of Animal Models for Human Diseases, Changchun, Jilin China

[6 ]International Center of Future Science, Jilin University, ( https://ror.org/00js3aw79) Changchun, Jilin China

[7 ]State Key Laboratory of Supramolecular Structure and Materials, Jilin University, ( https://ror.org/00js3aw79) Changchun, Jilin China

Article

Publisher ID: 3195

DOI: 10.1186/s12951-025-03195-3

PMC ID: 11800495

SO-VID: 6887c7ba-9343-49e3-80c5-dd6771c68ab0

License:

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.

History

Date received : 30 October 2024

Date accepted : 2 February 2025

Funding

Funded by: Science and Technology Development Program Project of Jilin Province

Award ID: YDZJ202301ZYTS063

Award ID: YDZJ202401284ZYTS

Award Recipient : Haisong Li Shuhan Liu

Funded by: Talent Reserve Program (TRP) of the First Hospital of Jilin University

Award ID: JDYYCB-2023008

Award Recipient : Shuhan Liu

Funded by: Youth Development Fund of the First Hospital of Jilin University

Award ID: JDYY14202305

Award Recipient : Shuhan Liu

Funded by: Health Science and Technology Capacity Enhancement Program of Jilin Province

Award ID: 2022JC056

Award Recipient : Shuhan Liu

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ScienceOpen disciplines: Biotechnology

Keywords: neutrophil extracellular traps (nets),nanoparticle (np),drug delivery,neutrophils,net modulation

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ScienceOpen disciplines: Biotechnology

Keywords: neutrophil extracellular traps (nets), nanoparticle (np), drug delivery, neutrophils, net modulation

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Innovative nanoparticle-based approaches for modulating neutrophil extracellular traps in diseases: from mechanisms to therapeutics

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RNA drug delivery

Most cited references 181

Neutrophil extracellular traps kill bacteria.

Neutrophil extracellular traps in immunity and disease

Platelet TLR4 activates neutrophil extracellular traps to ensnare bacteria in septic blood.

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