Resolvin D2 recovers neural injury by suppressing inflammatory mediators expression in lipopolysaccharide-induced Parkinson's disease rat model

Tian, Yiming; Zhang, Ying; Zhang, Ruoyu; Qiao, Shan; Fan, Jing

doi:10.1016/j.bbrc.2015.03.109

Cited by 56 publications

(57 citation statements)

References 20 publications

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“…RvD2 is a potent immunoresolvent that stereoselectively reduces excessive PMN trafficking in peritonitis and improves survival in sepsis (19). RvD2’s potent nanogram actions are also protective in disease models where RvD2 prevents inflammatory bowel disease such as colitis (22), alleviates inflammatory and fibromyalgia-induced pain (23, 24), increases survival following burn wound and reduces kidney and liver injuries in mice (25, 26), periodontitis (27) as well as nerve injuries as seen in Parkinson’s disease (28). …”

Section: Introductionmentioning

confidence: 99%

Novel Resolvin D2 Receptor Axis in Infectious Inflammation

Chiang

Rosa

Libreros

et al. 2017

The Journal of Immunology

135

124

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Resolution of acute inflammation is an active process governed by specialized pro-resolving mediators (SPM) including resolvin D2 (RvD2) that activates a cell surface G protein–coupled receptor (GPCR), GPR18/DRV2. Here, we investigated RvD2-DRV2-dependent resolution mechanisms using DRV2-deficient mice (DRV2-KO). In polymicrobial sepsis initiated by cecal ligation and puncture (CLP), RvD2 (~2.7 nmol/mouse) significantly increased survival (>50%) of wild-type (WT), reduced hypothermia and bacterial titers compared to vehicle-treated CLP mice that succumbed at 48h. Protection by RvD2 was abolished in DRV2-KO mice. Mass spectrometry-based lipid mediator metabololipidomics demonstrated that DRV2-KO infectious exudates gave higher pro-inflammatory leukotriene (LT) B4 and pro-coagulating thromboxane (TX) B2, as well as lower SPM, including RvD1 and RvD3, compared to WT. RvD2-DRV2-initiated intracellular signals were investigated using mass cytometry (CyTOF) which demonstrated that RvD2 enhanced phosphorylation of CREB, ERK1/2 and STAT3 that were absent in DRV2-KO macrophages. Monitored by real-time imaging, RvD2-DRV2 interaction significantly enhanced phagocytosis of live E. coli, an action dependent on PKA and STAT3 in macrophages. Taken together, we identified an RvD2-DRV2 axis that activates intracellular signaling pathways that increase phagocytosis-mediated bacterial clearance, survival and organ protection. Moreover, these results provide evidence for RvD2-DRV2 and their downstream pathways in pathophysiology of infectious inflammation.

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Section: Introductionmentioning

confidence: 99%

Novel Resolvin D2 Receptor Axis in Infectious Inflammation

Chiang

Rosa

Libreros

et al. 2017

The Journal of Immunology

135

124

View full text Add to dashboard Cite

show abstract

“…31 Furthermore, resolving mediators, particularly RVD1 and MaR1, have been shown to suppress NF-κB activation in cells such as microglia, 32,33 smooth muscle cells 34 and vascular endothelial cells, 35 as well as in several inflammatory disease animal models, including acute lung injury, 15,18,36 colitis 19 and sepsis. 37 However, the events leading to inhibition of NF-κB signaling have yet to be fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Resolvin D1, resolvin D2 and maresin 1 activate the GSK3β anti-inflammatory axis in TLR4-engaged human monocytes

Lamont

et al. 2016

Innate Immun

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Pro-resolving, docosahexaenoic acid-derived mediators have recently emerged as important potential therapeutic agents for the amelioration of complications arising from inflammation, such as vascular disease, asthma, acute lung injury and colitis. While resolvin D1 (RVD1), resolvin D2 (RVD2) and maresin 1 (MaR1) are established pro-resolvins, their mechanisms of action remain unclear. Here we show that, in LPS-stimulated primary human monocytes, RVD1, RVD2 and MaR1 each suppress the release of pro-inflammatory cytokines (TNF, IL-1β, IL-8) and the innate/adaptive bridging cytokine, IL-12 p40, while simultaneously augmenting the production of the anti-inflammatory cytokine, IL-10. Such resolving activity is accompanied by the increased phosphorylation (enhanced anti-inflammatory state) of glycogen synthase kinase 3β (GSK3β) along with increased phosphorylation (activation) of Akt, SGK1 and CREB but not MAPK-related molecules. Gain and loss of function experiments confirm a key role for GSK3β and CREB in the anti-inflammatory actions of resolvins. These results suggest that induction of the GSK3β anti-inflammatory axis is a common mechanism of action for RVD1, RVD2 and MaR1.

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“…Many natural and/or endogenous compounds have recently been shown to be effective in rodent models of PD as well, such as resveratrol [26–28], tanshinone [29,30], silymarin [31–35], resolvins [36], diadzein [37], and apocynin derivatives [38,39]. The majority of these compounds act as both anti-inflammatory agents as well as anti-oxidants.…”

Section: Introductionmentioning

confidence: 99%

Immunomodulation as a neuroprotective and therapeutic strategy for Parkinson's disease

Olson

Gendelman²

2016

Current Opinion in Pharmacology

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While immune control is associated with nigrostriatal neuroprotection for Parkinson’s disease, direct cause and effect relationships have not yet been realized, and modulating the immune system for therapeutic gain has been openly debated. Here, we review how innate and adaptive immunity affect disease pathobiology, and how each could be harnessed for treatment. The overarching idea is to employ immunopharmacologics as neuroprotective strategies for disease. The aim of the current work is to review disease-modifying treatments that are currently being developed as neuroprotective strategies for PD in experimental animal models and for human disease translation. The long-term goal of this research is to effectively harness the immune system to slow or prevent PD pathobiology.

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Resolvin D2 recovers neural injury by suppressing inflammatory mediators expression in lipopolysaccharide-induced Parkinson's disease rat model

Cited by 56 publications

References 20 publications

Novel Resolvin D2 Receptor Axis in Infectious Inflammation

Novel Resolvin D2 Receptor Axis in Infectious Inflammation

Resolvin D1, resolvin D2 and maresin 1 activate the GSK3β anti-inflammatory axis in TLR4-engaged human monocytes

Immunomodulation as a neuroprotective and therapeutic strategy for Parkinson's disease

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