The role of mtDAMPs in the trauma-induced systemic inflammatory response syndrome

Ye, Jingjing; Hu, Xiaodan; Wang, Zhiwei; Li, Rui; Gan, Lebin; Zhang, Mengwei; Wang, Tianbing

doi:10.3389/fimmu.2023.1164187

Cited by 12 publications

(3 citation statements)

References 144 publications

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“…According to previous studies, mtDNA is released into the joint fluids in rheumatoid arthritis [ 7 ] and released into circulation in trauma [ 10 ], acute respiratory distress syndrome, sepsis, and systemic inflammatory response syndrome, and the increased level of circulating mtDNA is associated with high mortality [ 14 , 17 ]. In this study, we observed a significant positive correlation between cell death and extracellular mtDNA levels, as well as between the extracellular mtDNA and inflammatory cytokine levels in hyperoxia-exposed newborn rat lungs.…”

Section: Discussionmentioning

confidence: 99%

Mesenchymal Stem Cells Reduce the Extracellular Mitochondrial DNA-Mediated TLR9 Activation in Neonatal Hyperoxia-Induced Lung Injury

Kim,

Ahn,

Sung

et al. 2024

Biomedicines

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Mitochondrial DNA (mtDNA) released from dead or injured cells can activate inflammation, and mesenchymal stem cell (MSC) transplantation can reduce inflammation and injury. However, it has not been tested whether the release of mtDNA can be reduced by MSC transplantation. We hypothesized that the level of extracellular mtDNA would be increased after hyperoxia-induced lung injury but reduced after lung injury attenuation by MSC therapy in our newborn rat model. In an in vitro study using a rat lung epithelial L2 cell line, we found that the level of extracellular mtDNA was significantly increased with H2O2-induced cell death but reduced after MSC co-incubation. In an in vivo study, we confirmed that the levels of cell death, extracellular mtDNA, and inflammatory cytokines were significantly increased in hyperoxic newborn rat lungs but reduced after MSC transplantation. The levels of extracellular mtDNA were significantly and positively correlated with the levels of the inflammatory cytokines. The TLR9/MyD88/NF-κB pathway, which is activated by binding to mtDNA, was also significantly upregulated but downregulated after MSC transplantation. We found a significant positive correlation between inflammatory cytokines and extracellular mtDNA in intubated neonates. The levels of inflammatory cytokines and extracellular mtDNA changed over time in a similar pattern in transtracheal aspirate samples from intubated neonates. In conclusion, increased levels of extracellular mtDNA are associated with increased inflammation in hyperoxia-induced lung injury, and attenuation of lung inflammation by MSC therapy is associated with reduced levels of extracellular mtDNA.

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Section: Discussionmentioning

confidence: 99%

Mesenchymal Stem Cells Reduce the Extracellular Mitochondrial DNA-Mediated TLR9 Activation in Neonatal Hyperoxia-Induced Lung Injury

Kim,

Ahn,

Sung

et al. 2024

Biomedicines

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“…TBI occurs when an external mechanical force impacts the head, leading to temporary or permanent impairments in brain function ( Jenkins, 2023 ). TBI could be of forms, i.e., primary and secondary phases of damages ( Ye et al, 2023 ). The primary injury induced immediately by the external force causes tissue damage through skull fractures, haemorrhages, and vascular injury ( Xiong et al, 2013 ).…”

Section: Role Of Phytochemicals In Tbimentioning

confidence: 99%

“…EGCG also reduces neutrophil infiltration and proinflammatory cytokine production after TBI ( Zeng et al, 2023 ). EGCG remarkably attenuates neuronal apoptosis in the hippocampus induced by TBI by upregulating Bcl-2, downregulating Bax, and cleaved caspase-3 expression ( Ye et al, 2023 ). It also reduces apoptosis by activating the Nrf2 signaling pathway and inducing antioxidant enzymes.…”

Section: Role Of Phytochemicals In Tbimentioning

confidence: 99%

The neuroprotective potential of phytochemicals in traumatic brain injury: mechanistic insights and pharmacological implications

Hasan,

Anwar,

Shamsi

et al. 2024

Front. Pharmacol.

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Traumatic brain injury (TBI) leads to brain damage, comprising both immediate primary damage and a subsequent cascade of secondary injury mechanisms. The primary injury results in localized brain damage, while the secondary damage initiates inflammatory responses, followed by the disruption of the blood-brain barrier, infiltration of peripheral blood cells, brain edema, and the release of various immune mediators, including chemotactic factors and interleukins. TBI disrupts molecular signaling, cell structures, and functions. In addition to physical tissue damage, such as axonal injuries, contusions, and haemorrhages, TBI interferes with brain functioning, impacting cognition, decision-making, memory, attention, and speech capabilities. Despite a deep understanding of the pathophysiology of TBI, an intensive effort to evaluate the underlying mechanisms with effective therapeutic interventions is imperative to manage the repercussions of TBI. Studies have commenced to explore the potential of employing natural compounds as therapeutic interventions for TBI. These compounds are characterized by their low toxicity and limited interactions with conventional drugs. Moreover, many natural compounds demonstrate the capacity to target various aspects of the secondary injury process. While our understanding of the pathophysiology of TBI, there is an urgent need for effective therapeutic interventions to mitigate its consequences. Here, we aimed to summarize the mechanism of action and the role of phytochemicals against TBI progression. This review discusses the therapeutic implications of various phytonutrients and addresses primary and secondary consequences of TBI. In addition, we highlighted the roles of emerging phytochemicals as promising candidates for therapeutic intervention of TBI. The review highlights the neuroprotective roles of phytochemicals against TBI and the mechanistic approach. Furthermore, our efforts focused on the underlying mechanisms, providing a better understanding of the therapeutic potential of phytochemicals in TBI therapeutics.

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Oxidative Stress and Inflammation in Myocardial Ischemia–Reperfusion Injury: Protective Effects of Plant‐Derived Natural Active Compounds

Chen,

Wang,

Meng

et al. 2024

J of Applied Toxicology

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Acute myocardial infarction (AMI) remains a leading cause of death among patients with cardiovascular diseases. Percutaneous coronary intervention (PCI) has been the preferred clinical treatment for AMI due to its safety and efficiency. However, research indicates that the rapid restoration of myocardial oxygen supply following PCI can lead to secondary myocardial injury, termed myocardial ischemia–reperfusion injury (MIRI), posing a grave threat to patient survival. Despite ongoing efforts, the mechanisms underlying MIRI are not yet fully elucidated. Among them, oxidative stress and inflammation stand out as critical pathophysiological mechanisms, playing significant roles in MIRI. Natural compounds have shown strong clinical therapeutic potential due to their high efficacy, availability, and low side effects. Many current studies indicate that natural compounds can mitigate MIRI by reducing oxidative stress and inflammatory responses. Therefore, this paper reviews the mechanisms of oxidative stress and inflammation during MIRI and the role of natural compounds in intervening in these processes, aiming to provide a basis and reference for future research and development of drugs for treating MIRI.

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The role of mtDAMPs in the trauma-induced systemic inflammatory response syndrome

Cited by 12 publications

References 144 publications

Mesenchymal Stem Cells Reduce the Extracellular Mitochondrial DNA-Mediated TLR9 Activation in Neonatal Hyperoxia-Induced Lung Injury

Mesenchymal Stem Cells Reduce the Extracellular Mitochondrial DNA-Mediated TLR9 Activation in Neonatal Hyperoxia-Induced Lung Injury

The neuroprotective potential of phytochemicals in traumatic brain injury: mechanistic insights and pharmacological implications

Oxidative Stress and Inflammation in Myocardial Ischemia–Reperfusion Injury: Protective Effects of Plant‐Derived Natural Active Compounds

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