Neutrophil Extracellular Trap Density Increases With Increasing Histopathological Severity of Crohn’s Disease

Schroder, Angie L; Chami, Belal; Liu, Yuyang; Doyle, Chloe; Kazzi, Mary El; Ahlenstiel, Golo; Ahmad, Gulfam; Pathma‐Nathan, Nimalan; Collins, Geoff; Toh, James Wei Tatt; Harman, Andrew N.; Byrne, Scott N.; Ctercteko, Grahame; Witting, Paul K.

doi:10.1093/ibd/izab239

Cited by 21 publications

(13 citation statements)

References 61 publications

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“…With downregulation of the CD98 gene, gut homeostasis was maintained, and the susceptibility of mice to DSS-induced colitis was decreased; both would be beneficial to inflammation resolution. Myeloperoxidase (MPO), whose activity could reflect the degree of neutrophil infiltration at inflammatory sites, could be used for evaluating the severity of UC . After DSS induction, MPO activity was increased, while CNZM, CPZM, and CCZM treatment decreased the MPO activity, in which CCZM treatment exerted the best effect (Figure F).…”

Section: Resultsmentioning

confidence: 99%

“…Myeloperoxidase (MPO), whose activity could reflect the degree of neutrophil infiltration at inflammatory sites, could be used for evaluating the severity of UC. 44 After DSS induction, MPO activity was increased, while CNZM, CPZM, and CCZM treatment decreased the MPO activity, in which CCZM treatment exerted the best effect (Figure 7F). This result demonstrated that after treatment, the neutrophil infiltration was decreased, and the severity of UC was mitigated.…”

Section: Cell Internalization Of Biomimetic Mofsmentioning

confidence: 92%

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Biomimetic MOF Nanoparticles Delivery of C-Dot Nanozyme and CRISPR/Cas9 System for Site-Specific Treatment of Ulcerative Colitis

Gao

Zhang

et al. 2022

ACS Appl. Mater. Interfaces

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Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) of unknown etiology affecting the colon and rectum. Previous studies have found that reactive oxygen species (ROS) overproduction and transmembrane glycoprotein CD98 (encoded by SLC3A2) upregulation played important roles in the initiation and progression of UC. On the basis of this, a biomimetic pH-responsive metal organic framework (MOF) carrier was constructed to deliver carbon nanodot-SOD nanozyme and clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) (CRISPR/Cas9) system for site-specific treatment of UC. In this system, carbon nanodots (C-dots) and CD98 CRISPR/Cas9 plasmid were successfully encapsulated into MOF carrier (ZIF-8 nanoparticles) by a one-pot approach (formed as CCZ), and then camouflaged with macrophage membrane (formed as CCZM). It was worth noting that the C-dot nanozyme showed excellent superoxide dismutase (SOD) enzymatic activity, which could scavenge ROS effectively. As expected, this biomimetic system exhibited pH-responsive, immune escape, and inflammation targeting capability simultaneously. In vitro experiments showed that ROS was significantly eliminated, and CD98 was downregulated by CCZM. In the dextran sulfate sodium salt (DSS)-induced UC model, administration of CCZM significantly ameliorated the inflammation symptoms of mice, including the colon length and pathological parameters such as epithelium integrity and inflammation infiltration. In addition, both in vitro and in vivo results demonstrated that biomimetic nanoparticles effectively reduced the expression of pro-inflammatory cytokines. Overall, this study would provide a promising approach for the precise treatment of UC.

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Section: Resultsmentioning

confidence: 99%

Section: Cell Internalization Of Biomimetic Mofsmentioning

confidence: 92%

Biomimetic MOF Nanoparticles Delivery of C-Dot Nanozyme and CRISPR/Cas9 System for Site-Specific Treatment of Ulcerative Colitis

Gao

Zhang

et al. 2022

ACS Appl. Mater. Interfaces

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“…Extensive studies have confirmed that uncontrolled and excessive NETs are involved in the pathogenesis of autoimmune disease ( 10 , 11 ), cardiovascular disease ( 12 ), inflammatory disease ( 13 ) and cancer ( 14 ). It is worth mentioning that the function of NETs in tumors is gradually expanding.…”

Section: Introductionmentioning

confidence: 99%

Neutrophil extracellular traps in tumor progression and immunotherapy

Yan

Sun

et al. 2023

Front. Immunol.

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Tumor immunity is a growing field of research that involves immune cells within the tumor microenvironment. Neutrophil extracellular traps (NETs) are neutrophil-derived extracellular web-like chromatin structures that are composed of histones and granule proteins. Initially discovered as the predominant host defense against pathogens, NETs have attracted increasing attention due to they have also been tightly associated with tumor. Excessive NET formation has been linked to increased tumor growth, metastasis, and drug resistance. Moreover, through direct and/or indirect effects on immune cells, an abnormal increase in NETs benefits immune exclusion and inhibits T-cell mediated antitumor immune responses. In this review, we summarize the recent but rapid progress in understanding the pivotal roles of NETs in tumor and anti-tumor immunity, highlighting the most relevant challenges in the field. We believe that NETs may be a promising therapeutic target for tumor immunotherapy.

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“…Moreover, NETs could promote gastric cancer cell proliferation, invasion, migration and epithelial–mesenchymal transition dependent on TGF-β signaling [ 23 ]. Furthermore, it has been proved that TNF-α up-regulated neutrophil elastase in vascular smooth muscle cells (VSMCs), which promoted VSMC migration, proliferation and inflammation [ 24 ] and mediates the formation of NETs [ 25 ]. VSMC proliferation is one of the key vascular pathological changes occurring during the development of hypertension [ 26 ].…”

Section: Introductionmentioning

confidence: 99%

Neutrophil extracellular traps accelerate vascular smooth muscle cell proliferation via Akt/CDKN1b/TK1 accompanying with the occurrence of hypertension

Fang

Li²,

Yan³

et al. 2022

Journal of Hypertension

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Objective: Neutrophil extracellular traps (NETs) can trigger pathological changes in vascular cells or vessel wall components, which are vascular pathological changes of hypertension. Therefore, we hypothesized that NETs would be associated with the occurrence of hypertension. Methods: To evaluate the relationship between NETs and hypertension, we evaluated both the NETs formation in spontaneously hypertensive rats (SHRs) and the blood pressure of mice injected phorbol-12-myristate-13-acetate (PMA) via the tail vein to induce NETs formation in arterial wall. Meanwhile, proliferation and cell cycle of vascular smooth muscle cells (VSMCs), which were co-cultured with NETs were assessed. In addition, the role of exosomes from VSMCs co-cultured with NETs on proliferation signaling delivery was assessed. Results: Formation of NETs increased in the arteries of SHR. PMA resulted in up-regulation expression of citrullinated Histone H3 (cit Histone H3, a NETs marker) in the arteries of mice accompanied with increasing of blood pressure. NET treatment significantly increased VSMCs count and accelerated G1/S transition in vitro . Cyclin-dependent kinase inhibitor 1b (CDKN1b) was down-regulated and Thymidine kinase 1 (TK1) was up-regulated in VSMCs. Exosomes from VSMCs co-cultured with NETs significantly accelerated the proliferation of VSMCs. TK1 was up-regulated in the exosomes from VSMCs co-cultured with NETs and in both the arterial wall and serum of mice with PMA. Conclusion: NETs promote VSMCs proliferation via Akt/CDKN1b/TK1 and is related to hypertension development. Exosomes from VSMCs co-cultured with NETs participate in transferring the proliferation signal. These results support the role of NETs in the development of hypertension.

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Neutrophil Extracellular Trap Density Increases With Increasing Histopathological Severity of Crohn’s Disease

Cited by 21 publications

References 61 publications

Biomimetic MOF Nanoparticles Delivery of C-Dot Nanozyme and CRISPR/Cas9 System for Site-Specific Treatment of Ulcerative Colitis

Biomimetic MOF Nanoparticles Delivery of C-Dot Nanozyme and CRISPR/Cas9 System for Site-Specific Treatment of Ulcerative Colitis

Neutrophil extracellular traps in tumor progression and immunotherapy

Neutrophil extracellular traps accelerate vascular smooth muscle cell proliferation via Akt/CDKN1b/TK1 accompanying with the occurrence of hypertension

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