Inhibition of TREM1 reduces inflammation and oxidative stress after spinal cord injury (SCI) associated with HO-1 expressions

Li, Zhenhuan; Wu, Fuqiang; Xu, Dafeng; Zhi, Zhongzheng; Xu, Guanghui

doi:10.1016/j.biopha.2018.08.159

Cited by 77 publications

(54 citation statements)

References 35 publications

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“…However, as reported by a clinical study on UC patients, the increase in sTREM-1 is not to be necessarily related to bacterial infections, since patients with infectious colitis were excluded from the study and blood cultures were found to be sterile [23]. As support, TREMs are implicated even in sterile inflammatory-related conditions, including neurodegenerative disorders, such as AD, Parkinson’s disease (PD), Multiple Sclerosis (MS), and stroke, among others [12,13,14,24,25,26,27,28,29]. It is remarkable that a vast body of evidence is emerging, indicating that bowel inflammation is bound to the pathogenesis of CNS disorders.…”

Section: Microbiota and Gastrointestinal Diseasesmentioning

confidence: 99%

“…TREM-1 expression is augmented in the injured spinal cord of mice models [24]. Conversely, TREM-1 ablation leads to improved locomotor function and reduced levels of peripheral nerve injury-related biomarkers and inflammation-related regulators in the murine spinal cord.…”

Section: Role Of Trems In Neurodegenerative Disordersmentioning

confidence: 99%

“…Conversely, TREM-1 ablation leads to improved locomotor function and reduced levels of peripheral nerve injury-related biomarkers and inflammation-related regulators in the murine spinal cord. In detail, TREM-1 ablation leads to a down-regulation of TLR-2, -3, -4, and -9, NF-κB, and oxidative stress markers, while enhancing anti-oxidants, such as superoxide dismutase-1 (SOD1), NAD(P)H:quinone oxidoreductase-1 (NQO-1), heme oxygenase-1 (HO-1), and nuclear factor E2-related factor 2 (Nrf2) in the injured spinal cord [24]. These results are reproduced in vitro following LPS administration, where a predominant role for HO-1 emerged.…”

Section: Role Of Trems In Neurodegenerative Disordersmentioning

confidence: 99%

“…These results are reproduced in vitro following LPS administration, where a predominant role for HO-1 emerged. HO-1 suppression occludes the reduction in inflammation, oxidative stress, and glial cells activation, which is produced by TREM-1 ablation [24].…”

Section: Role Of Trems In Neurodegenerative Disordersmentioning

confidence: 99%

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TREM Receptors Connecting Bowel Inflammation to Neurodegenerative Disorders

Natale

Biagioni

Busceti

et al. 2019

Cells

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Alterations in Triggering Receptors Expressed on Myeloid cells (TREM-1/2) are bound to a variety of infectious, sterile inflammatory, and degenerative conditions, ranging from inflammatory bowel disease (IBD) to neurodegenerative disorders. TREMs are emerging as key players in pivotal mechanisms often concurring in IBD and neurodegeneration, namely microbiota dysbiosis, leaky gut, and inflammation. In conditions of dysbiosis, compounds released by intestinal bacteria activate TREMs on macrophages, leading to an exuberant pro-inflammatory reaction up to damage in the gut barrier. In turn, TREM-positive activated macrophages along with inflammatory mediators may reach the brain through the blood, glymphatic system, circumventricular organs, or the vagus nerve via the microbiota-gut-brain axis. This leads to a systemic inflammatory response which, in turn, impairs the blood-brain barrier, while promoting further TREM-dependent neuroinflammation and, ultimately, neural injury. Nonetheless, controversial results still exist on the role of TREM-2 compared with TREM-1, depending on disease specificity, stage, and degree of inflammation. Therefore, the present review aimed to provide an update on the role of TREMs in the pathophysiology of IBD and neurodegeneration. The evidence here discussed the highlights of the potential role of TREMs, especially TREM-1, in bridging inflammatory processes in intestinal and neurodegenerative disorders.

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Section: Microbiota and Gastrointestinal Diseasesmentioning

confidence: 99%

Section: Role Of Trems In Neurodegenerative Disordersmentioning

confidence: 99%

Section: Role Of Trems In Neurodegenerative Disordersmentioning

confidence: 99%

Section: Role Of Trems In Neurodegenerative Disordersmentioning

confidence: 99%

See 2 more Smart Citations

TREM Receptors Connecting Bowel Inflammation to Neurodegenerative Disorders

Natale

Biagioni

Busceti

et al. 2019

Cells

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“…Oxidative stress has been reported to participate in and accelerate secondary injury processing in spinal cord injury after the physical trauma to the spinal cord [34,35]. Therefore, suppression of oxidative stress has been considered as an effective therapeutic strategy to improve SCI recovery.…”

Section: Discussionmentioning

confidence: 99%

Tauroursodeoxycholic Acid Alleviates Secondary Injury in Spinal Cord Injury Mice Through Reducing Oxidative Stress, Apoptosis, and Inflammatory Response

Hou

Luan

Deng

et al. 2021

Preprint

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Background Tauroursodeoxycholic acid (TUDCA) is a hydrophilic bile acid derivative, which has been demonstrated to have neuroprotective effects in different neurological disease models. However, the effect and underlying mechanism of TUDCA on spinal cord injury (SCI) have not been fully elucidated. This study is aim to investigate the protective effects of TUDCA in SCI mouse model and the related mechanism involved.Methods The primary cortical neurons were isolated from E16.5 C57BL/6 mouse embryos. To evaluate the effect of TUDCA on oxidative stress in vitro, the cortical neurons were treated with H2O2 with or without TUDCA added. Mice were randomly divided into sham, SCI and TUDCA groups. SCI model was induced using a pneumatic impact device at T9-T10 level of vertebra. TUDCA (200 mg/kg) or equal volume of saline was intragastrically administrated daily post injury for 14 days. ResultsWe found that TUDCA reduced reactive oxygen species (ROS) generation, lactate dehydrogenase (LDH) release and restored superoxide dismutase (SOD) activity to protect primary cortical neurons from oxidative stress in vitro. In vivo, TUDCA treatment significantly reduced tissue injury, oxidative stress, inflammatory response, and apoptosis; promoted axon regeneration and remyelination in the lesion site of spinal cord of SCI mice. The functional recovery test revealed that TUDCA treatment significantly ameliorated recovery of limb function.ConclusionsTUDCA treatment can alleviate secondary injury and promote functional recovery through reducing oxidative stress, inflammatory response and apoptosis induced by primary injury, and promote axon regeneration and remyelination, which could be used as a potential therapy for human SCI recovery.

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Effect of electroacupuncture on inhibition of inflammatory response and oxidative stress through activating ApoE and Nrf2 in a mouse model of spinal cord injury

et al. 2021

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Introduction: Electroacupuncture protects neurons and myelinated axons after spinal cord injury by mitigating the inflammatory response and oxidative stress, but how it exerts these effects is unclear.Methods and results: Spinal cord injury was induced in C57BL/6 wild-type and apolipoprotein E (ApoE) knockout (ApoE -/-) mice, followed by electroacupuncture or ApoE mimetic peptide COG112 treatment. Mice with spinal cord injury suffered loss of myelinated axons and hindlimb motor function through the detections of Basso mouse scale, histology, and transmission electron microscopy; electroacupuncture partially reversed these effects in wild-type mice but not in ApoE -/mice. Combining exogenous ApoE administration with electroacupuncture significantly mitigated the effects of spinal cord injury in both mouse strains, and these effects were associated with up-regulation of anti-inflammatory cytokines and down-regulation of proinflammatory cytokines which were detected by quantitative reverse transcriptionpolymerase chain reaction. Combination treatment also reduced oxidative stress by up-regulating ApoE and Nrf2/HO-1 signaling pathway through the detections of immunofluorescence and western blot analysis. Conclusions:These results suggest that electroacupuncture protects neurons and myelinated axons following spinal cord injury through an ApoE-dependent mechanism.

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Inhibition of TREM1 reduces inflammation and oxidative stress after spinal cord injury (SCI) associated with HO-1 expressions

Cited by 77 publications

References 35 publications

TREM Receptors Connecting Bowel Inflammation to Neurodegenerative Disorders

TREM Receptors Connecting Bowel Inflammation to Neurodegenerative Disorders

Tauroursodeoxycholic Acid Alleviates Secondary Injury in Spinal Cord Injury Mice Through Reducing Oxidative Stress, Apoptosis, and Inflammatory Response

Effect of electroacupuncture on inhibition of inflammatory response and oxidative stress through activating ApoE and Nrf2 in a mouse model of spinal cord injury

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