The role of neutrophil extracellular traps in sepsis and sepsis-related acute lung injury

Zou, Shujing; Jie, Hongyu; Han, Xinai; Wang, Jinghong

doi:10.1016/j.intimp.2023.110436

Cited by 13 publications

(6 citation statements)

References 120 publications

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“…Moreover, mounting evidence suggests that NETosis is increased in both infectious and sterile ALI conditions [32]. Excessive NET release promotes thrombus formation, activates endothelial cells, and induces microvascular injury, resulting in heightened vascular permeability, intra-alveolar accumulation of protein-rich fluid, and inflammatory cell infiltration [33]. In our current investigation, we initially established that corilagin treatment effectively reduces NET formation in PMA-or LPS-activated human neutrophils.…”

Section: Discussionmentioning

confidence: 70%

Corilagin Inhibits Neutrophil Extracellular Trap Formation and Protects against Hydrochloric Acid/Lipopolysaccharide-Induced Acute Lung Injury in Mice by Suppressing the STAT3 and NOX2 Signaling Pathways

Liu,

Yu,

Liao

et al. 2024

Antioxidants

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Acute lung injury (ALI) and its severe manifestation, acute respiratory distress syndrome (ARDS), are characterized by uncontrolled inflammatory responses, neutrophil activation and infiltration, damage to the alveolar capillary membrane, and diffuse alveolar injury. Neutrophil extracellular traps (NETs), formed by activated neutrophils, contribute significantly to various inflammatory disorders and can lead to tissue damage and organ dysfunction. Corilagin, a compound found in Phyllanthus urinaria, possesses antioxidative and anti-inflammatory properties. In this study, we investigated the protective effects and underlying mechanisms of corilagin in hydrochloric acid (HCl)/lipopolysaccharide (LPS)-induced lung injury. Mice received intraperitoneal administration of corilagin (2.5, 5, or 10 mg/kg) or an equal volume of saline 30 min after intratracheal HCl/LPS administration. After 20 h, lung tissues were collected for analysis. Corilagin treatment significantly mitigated lung injury, as evidenced by reduced inflammatory cell infiltration, decreased production of proinflammatory cytokines, and alleviated oxidative stress. Furthermore, corilagin treatment suppressed neutrophil elastase expression, reduced NET formation, and inhibited the expression of ERK, p38, AKT, STAT3, and NOX2. Our findings suggest that corilagin inhibits NET formation and protects against HCl/LPS-induced ALI in mice by modulating the STAT3 and NOX2 signaling pathways.

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Section: Discussionmentioning

confidence: 70%

Corilagin Inhibits Neutrophil Extracellular Trap Formation and Protects against Hydrochloric Acid/Lipopolysaccharide-Induced Acute Lung Injury in Mice by Suppressing the STAT3 and NOX2 Signaling Pathways

Liu,

Yu,

Liao

et al. 2024

Antioxidants

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“…Our studies proved that the level of TNF-α and IL-1β effectively decreased in the supernatant of THP-1-derived macrophages cocultured with different concentrations of Ce-MBGNs after stimulated with LPS. This may be because of the antioxidant properties of Ce ions, which effectively clear ROS and reduce the expression of related inflammatory factors (Zou et al, 2023). Subsequently, DPCs were cultured with this supernatant, and the RT-qPCR results (Figure 8b) showed that the expression of IL-1Ra increased, whereas the expression of IL-1 receptor, MMP9 and CTR, which are related to the further expansion of inflammation and osteoclast differentiation, decreased (Al-Natour et al, 2021;Sharma et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Anti‐inflammatory cerium‐containing nano‐scaled mesoporous bioactive glass for promoting regenerative capability of dental pulp cells

Duan,

Zheng,

et al. 2024

Int Endodontic J

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AimsThis study aimed to investigate the anti‐inflammatory and odontoblastic effects of cerium‐containing mesoporous bioactive glass nanoparticles (Ce‐MBGNs) on dental pulp cells as novel pulp‐capping agents.MethodologyCe‐MBGNs were synthesized using a post‐impregnation strategy based on the antioxidant properties of Ce ions and proposed the first use of Ce‐MBGNs for pulp‐capping application. The biocompatibility of Ce‐MBGNs was analysed using the CCK‐8 assay and apoptosis detection. Additionally, the reactive oxygen species (ROS) scavenging ability of Ce‐MBGNs was measured using the 2,7‐Dichlorofuorescin Diacetate (DCFH‐DA) probe. The anti‐inflammatory effect of Ce‐MBGNs on THP‐1 cells was further investigated using flow cytometry and quantitative real‐time polymerase chain reaction (RT‐qPCR). Moreover, the effect of Ce‐MBGNs on the odontoblastic differentiation of the dental pulp cells (DPCs) was assessed by combined scratch assays, RT‐qPCR, western blotting, immunocytochemistry, Alizarin Red S staining and tissue‐nonspecific alkaline phosphatase staining. Analytically, the secretions of tumour necrosis factor‐α (TNF‐α) and interleukin‐1β (IL‐1β) were detected with enzyme‐linked immunosorbent assay (ELISA).ResultsCe‐MBGNs were confirmed to effectively scavenge ROS in THP‐1‐derived macrophages and DPCs. Flow cytometry and RT‐qPCR assays revealed that Ce‐MBGNs significantly inhibited the M1 polarization of macrophages (Mφ). Furthermore, the protein levels of TNF‐α and IL‐1β were downregulated in THP‐1‐derived macrophages after stimulation with Ce‐MBGNs. With a step‐forward virtue of promoting the odontoblastic differentiation of DPCs, we further confirmed that Ce‐MBGNs could regulate the formation of a conductive immune microenvironment with respect to tissue repair in DPCs, which was mediated by macrophages.ConclusionsCe‐MBGNs protected cells from self‐produced oxidative damage and exhibited excellent immunomodulatory and odontoblastic differentiation effects on DPCs. As a pulp‐capping agent, this novel biomaterial can exert anti‐inflammatory effects and promote restorative dentine regeneration in clinical treatment. We believe that this study will stimulate further correlative research on the development of advanced pulp‐capping agents.

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“…NETs protect the host by trapping and killing pathogens. However, excessive NET formation can stimulate and synergize with other cells, leading to amplification of the cascade response to sterile inflammation, and these pathological processes can cause damage to the organism [ 86 , 87 ].…”

Section: Multiple Targets For Treating Alimentioning

confidence: 99%

Advances in nanomaterial-targeted treatment of acute lung injury after burns

Zhang,

Zhao,

Xue

et al. 2024

J Nanobiotechnol

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Acute lung injury (ALI) is a common complication in patients with severe burns and has a complex pathogenesis and high morbidity and mortality rates. A variety of drugs have been identified in the clinic for the treatment of ALI, but they have toxic side effects caused by easy degradation in the body and distribution throughout the body. In recent years, as the understanding of the mechanism underlying ALI has improved, scholars have developed a variety of new nanomaterials that can be safely and effectively targeted for the treatment of ALI. Most of these methods involve nanomaterials such as lipids, organic polymers, peptides, extracellular vesicles or cell membranes, inorganic nanoparticles and other nanomaterials, which are targeted to reach lung tissues to perform their functions through active targeting or passive targeting, a process that involves a variety of cells or organelles. In this review, first, the mechanisms and pathophysiological features of ALI occurrence after burn injury are reviewed, potential therapeutic targets for ALI are summarized, existing nanomaterials for the targeted treatment of ALI are classified, and possible problems and challenges of nanomaterials in the targeted treatment of ALI are discussed to provide a reference for the development of nanomaterials for the targeted treatment of ALI.

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The role of neutrophil extracellular traps in sepsis and sepsis-related acute lung injury

Cited by 13 publications

References 120 publications

Corilagin Inhibits Neutrophil Extracellular Trap Formation and Protects against Hydrochloric Acid/Lipopolysaccharide-Induced Acute Lung Injury in Mice by Suppressing the STAT3 and NOX2 Signaling Pathways

Corilagin Inhibits Neutrophil Extracellular Trap Formation and Protects against Hydrochloric Acid/Lipopolysaccharide-Induced Acute Lung Injury in Mice by Suppressing the STAT3 and NOX2 Signaling Pathways

Anti‐inflammatory cerium‐containing nano‐scaled mesoporous bioactive glass for promoting regenerative capability of dental pulp cells

Advances in nanomaterial-targeted treatment of acute lung injury after burns

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