Resolvin D1 promotes the interleukin-4-induced alternative activation in BV-2 microglial cells

Li, Longyan; Wu, Yan; Wang, Yanping; Wu, Jing; Song, Limin; Xian, Wenjing; Yuan, Shiying; Pei, Lei; Shang, You

doi:10.1186/1742-2094-11-72

Cited by 61 publications

(43 citation statements)

References 46 publications

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“…Binding separation of the protein DNA complexes from unbound DNA by electrophoresis was performed as previously described in detail (26). Nuclear protein after 1 h of S100A8/A9 treatment and a 200-fold molar excess of unlabeled consensus sequence were used as the specific competitor in the control lane.…”

Section: Methodsmentioning

confidence: 99%

Proinflammatory effects of S100A8/A9 via TLR4 and RAGE signaling pathways in BV-2 microglial cells

Sun

Zhang

et al. 2017

International Journal of Molecular Medicine

114

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S100A8/A9, a heterodimer of the two calcium-binding proteins S100A8 and S100A9, has emerged as an important proinflammatory mediator in acute and chronic inflammation. However, whether S100A8/A9 is implicated in microglial-induced neuroinflammatory response remains unclear. Here, we found that S100A8/A9 significantly increased the secretion of proinflammatory cytokines including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in cultured BV-2 microglial cells. Inhibition of the Toll-like receptor 4 (TLR4) and the receptor for advanced glycation end-products (RAGE) with C225 and a RAGE-blocking antibody, respectively significantly reduced the secretion of TNF-α and IL-6 from S100A8/A9-stimulated BV-2 microglial cells. Furthermore, S100A8/A9 markedly enhanced the nuclear translocation of NF-κB p65 and the DNA-binding activities of NF-κB in BV-2 microglial cells, and suppression of ERK and JNK/MAPK signaling pathways by PD98059 or SP600125 significantly inhibited NF-κB activity and the release of TNF-α and IL-6 in the S100A8/A9-treated BV-2 microglial cells. Our data also showed that inhibition of NF-κB with pyrrolidine dithiocarbamate (PDTC) significantly reduced the secretion of TNF-α and IL-6 from BV-2 microglial cells treated with S100A8/A9. Taken together, our data suggest that S100A8/A9 acts directly on BV-2 microglial cells via binding to TLR4 and RAGE on the membrane and then stimulates the secretion of proinflammatory cytokines through ERK and JNK-mediated NF-κB activity in BV-2 microglial cells. Targeting S100A8/A9 may provide a novel therapeutic strategy in microglial-induced neuroinflammatory diseases.

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Section: Methodsmentioning

confidence: 99%

Proinflammatory effects of S100A8/A9 via TLR4 and RAGE signaling pathways in BV-2 microglial cells

Sun

Zhang

et al. 2017

International Journal of Molecular Medicine

114

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“…We and others have reported that RvD1 promotes alternative activation of macrophages (the M2 phenotype) 11,50 and that the M2 macrophages appear to mitigate inflammation and promote the resolution of inflammation in acute models and cell culture systems. 11,51 However, some evidence suggests that in chronic diseases, M2 macrophages may promote tissue remodeling and repair, leading to fibrosis. 38 In our model of long-term smoke exposure with AT-RvD1 treatment, we did not find evidence of preferential M1 or M2 activation.…”

Section: Discussionmentioning

confidence: 99%

Resolvin D1 Reduces Emphysema and Chronic Inflammation

Hsiao

Thatcher

Colas

et al. 2015

The American Journal of Pathology

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Chronic obstructive pulmonary disease is characterized, in part, by chronic inflammation that persists even after smoking cessation, suggesting that a failure to resolve inflammation plays an important role in the pathogenesis of the disease. It is widely recognized that the resolution of inflammation is an active process, governed by specialized proresolving lipid mediators, including lipoxins, resolvins, maresins, and protectins. Here, we report that proresolving signaling and metabolic pathways are disrupted in lung tissue from patients with chronic obstructive pulmonary disease, suggesting that supplementation with proresolving lipid mediators might reduce the development of emphysema by controlling chronic inflammation. Groups of mice were exposed long-term to cigarette smoke and treated with the proresolving mediator resolvin D1. Resolvin D1 was associated with a reduced development of cigarette smokeeinduced emphysema and airspace enlargement, with concurrent reductions in inflammation, oxidative stress, and cell death. Interestingly, resolvin D1 did not promote the differentiation of M2 macrophages and did not promote tissue fibrosis. Taken together, our results suggest that cigarette smoking disrupts endogenous proresolving pathways and that supplementation with specialized proresolving lipid mediators is an important therapeutic strategy in chronic lung disease, especially if endogenous specialized proresolving lipid mediator signaling is impaired. (Am J Pathol 2015, 185: 3189e3201; http:// dx.doi.org/10.1016/j.ajpath.2015 Chronic obstructive pulmonary disease (COPD) is a major global health problem and a leading cause of death and disability. Tobacco smoking remains the major causative factor in the development of COPD; however, new evidence suggests that household air pollution from fuel used for indoor cooking and heating is also a significant cause.

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“…Thus, 2 SPMs 15-epi-LXA 4 and RvD1 were employed to determine their activity in modulating autophagy in macrophages. First, we incubated murine peritoneal macrophages with different concentrations of these pro-resolving lipids at concentration ranges at which they have previously been shown to activate significant pro-resolving actions 12,14,37 to determine the potential effects on MAP1LC3 processing (Fig. 1A).…”

Section: Introductionmentioning

confidence: 99%

Activation of autophagy in macrophages by pro-resolving lipid mediators

et al. 2015

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The resolution of inflammation is an active process driven by specialized pro-resolving lipid mediators, such as 15-epi-LXA4 and resolvin D1 (RvD1), that promote tissue regeneration. Macrophages regulate the innate immune response being key players during the resolution phase to avoid chronic inflammatory pathologies. Their half-life is tightly regulated to accomplish its phagocytic function, allowing the complete cleaning of the affected area. The balance between apoptosis and autophagy appears to be essential to control the survival of these immune cells within the inflammatory context. In the present work, we demonstrate that 15-epi-LXA4 and RvD1 at nanomolar concentrations promote autophagy in murine and human macrophages. Both compounds induced the MAP1LC3-I to MAP1LC3-II processing and the degradation of SQSTM1 as well as the formation of MAP1LC3(+) autophagosomes, a typical signature of autophagy. Furthermore, 15-epi-LXA4 and RvD1 treatment favored the fusion of the autophagosomes with lysosomes, allowing the final processing of the autophagic vesicles. This autophagic response involves the activation of MAPK1 and NFE2L2 pathways, but by an MTOR-independent mechanism. Moreover, these pro-resolving lipids improved the phagocytic activity of macrophages via NFE2L2. Therefore, 15-epi-LXA4 and RvD1 improved both survival and functionality of macrophages, which likely supports the recovery of tissue homeostasis and avoiding chronic inflammatory diseases.

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Resolvin D1 promotes the interleukin-4-induced alternative activation in BV-2 microglial cells

Cited by 61 publications

References 46 publications

Proinflammatory effects of S100A8/A9 via TLR4 and RAGE signaling pathways in BV-2 microglial cells

Proinflammatory effects of S100A8/A9 via TLR4 and RAGE signaling pathways in BV-2 microglial cells

Resolvin D1 Reduces Emphysema and Chronic Inflammation

Activation of autophagy in macrophages by pro-resolving lipid mediators

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