Resveratrol Induces the Expression of Interleukin-10 and  Brain-Derived Neurotrophic Factor in BV2 Microglia  under Hypoxia

Song, Jeong Sup; Cheon, So Yeong; Jung, Wonsug; Lee, Won Taek; Lee, Jong Eun

doi:10.3390/ijms150915512

Cited by 63 publications

(33 citation statements)

References 81 publications

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“…Other authors also found that hypoxia reduced basal and induced IL-10 protein and gene expressions 32 . Taken together, these data suggest that hypoxia significantly impairs IL-10 expression in macrophages, and this impairment is not ameliorated by MSCs.…”

Section: Discussionmentioning

confidence: 92%

Hypoxia impairs mesenchymal stromal cell-induced macrophage M1 to M2 transition

et al. 2017

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The transition of macrophages from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype is crucial for the progression of normal wound healing. Persistent M1 macrophages within the injury site may lead to an uncontrolled macrophage-mediated inflammatory response and ultimately a failure of the wound healing cascade, leading to chronic wounds. Mesenchymal stromal cells (MSCs) have been widely reported to promote M1 to M2 macrophage transition; however, it is unclear whether MSCs can drive this transition in the hypoxic environment typically observed in chronic wounds. Here we report on the effect of hypoxia (1% O2) on MSCs’ ability to transition macrophages from the M1 to the M2 phenotype. While hypoxia had no effect on MSC secretion, it inhibited MSC-induced M1 to M2 macrophage transition, and suppressed macrophage expression and production of the anti-inflammatory mediator interleukin-10 (IL-10). These results suggest that hypoxic environments may impede the therapeutic effects of MSCs.

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Section: Discussionmentioning

confidence: 92%

Hypoxia impairs mesenchymal stromal cell-induced macrophage M1 to M2 transition

et al. 2017

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“…Glatiramer acetate, an immunomodulatory agent used in relapsing-remitting multiple sclerosis, was shown to induce secretion of IL-10 by microglial cells [95]. Resveratrol administration to a microglial cell line prevented hypoxia-induced injury by up-regulating IL-10 and controlling inflammation [96]. Collectively, these reports show that the molecules present in the microenvironment can impact IL-10 production by microglia, thus shaping the outcome of the inflammatory response.…”

Section: Cellular Sources Of Il-10 In the Cnsmentioning

confidence: 99%

Balancing the immune response in the brain: IL-10 and its regulation

Lobo-Silva

Carriche

Castro

et al. 2016

J Neuroinflammation

327

199

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BackgroundThe inflammatory response is critical to fight insults, such as pathogen invasion or tissue damage, but if not resolved often becomes detrimental to the host. A growing body of evidence places non-resolved inflammation at the core of various pathologies, from cancer to neurodegenerative diseases. It is therefore not surprising that the immune system has evolved several regulatory mechanisms to achieve maximum protection in the absence of pathology.Main bodyThe production of the anti-inflammatory cytokine interleukin (IL)-10 is one of the most important mechanisms evolved by many immune cells to counteract damage driven by excessive inflammation. Innate immune cells of the central nervous system, notably microglia, are no exception and produce IL-10 downstream of pattern recognition receptors activation. However, whereas the molecular mechanisms regulating IL-10 expression by innate and acquired immune cells of the periphery have been extensively addressed, our knowledge on the modulation of IL-10 expression by central nervous cells is much scattered. This review addresses the current understanding on the molecular mechanisms regulating IL-10 expression by innate immune cells of the brain and the implications of IL-10 modulation in neurodegenerative disorders.ConclusionThe regulation of IL-10 production by central nervous cells remains a challenging field. Answering the many remaining outstanding questions will contribute to the design of targeted approaches aiming at controlling deleterious inflammation in the brain.

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“…Many studies showed that resveratrol treatment decreases inflammatory burden by reducing microglial activation in in vivo (Girbovan and Plamondon, 2015; Shin et al, 2010; Simao et al, 2012a) and in vitro (Song et al, 2014) models of ischemic stroke. Resveratrol has also been shown to reduce edema (Ren et al, 2011; Yousuf et al, 2009) and prevent the release of pro-inflammatory cytokines (Shin et al, 2010; Song et al, 2014). Furthermore, resveratrol alleviates inflammation by decreasing ROS levels which are known to activate immune cells (Khodr and Khalil, 2001).…”

Section: Anti-inflammatory Properties Of Resveratrolmentioning

confidence: 99%

Resveratrol neuroprotection in stroke and traumatic CNS injury

Lopez

Dempsey

Vemuganti

2015

Neurochemistry International

140

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Resveratrol, a stilbene formed in many plants in response to various stressors, elicits multiple beneficial effects in vertebrates. Particularly, resveratrol was shown to have therapeutic properties in cancer, atherosclerosis and neurodegeneration. Resveratrol-induced benefits are modulated by multiple synergistic pathways that control oxidative stress, inflammation and cell death. Despite the lack of a definitive mechanism, both in vivo and in vitro studies suggest that resveratrol can induce a neuroprotective state when administered acutely or prior to experimental injury to the CNS. In this review, we discuss the neuroprotective potential of resveratrol in stroke, traumatic brain injury and spinal cord injury, with a focus on the molecular pathways responsible for this protection.

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Resveratrol Induces the Expression of Interleukin-10 and Brain-Derived Neurotrophic Factor in BV2 Microglia under Hypoxia

Cited by 63 publications

References 81 publications

Hypoxia impairs mesenchymal stromal cell-induced macrophage M1 to M2 transition

Hypoxia impairs mesenchymal stromal cell-induced macrophage M1 to M2 transition

Balancing the immune response in the brain: IL-10 and its regulation

Resveratrol neuroprotection in stroke and traumatic CNS injury

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