|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Autophagy-mediated regulation of neutrophils and clinical applications显示文摘Autophagy,an adaptive catabolic process,plays a cytoprotective role in enabling cellular homeostasis in the innate and adaptive immune systems.Neutrophils,the most abundant immune cells in circulation,are professional killers that orchestrate a series of events during acute inflammation.The recent literature indicates that autophagy has important roles in regulating neutrophil functions,including differentiation,degranulation,metabolism and neutrophil extracellular trap formation,that dictate neutrophil fate.It is also becoming increasingly clear that autophagy regulation is critical for neutrophils to exert their immunological activity.However,evidence regarding the systematic communication between neutrophils and autophagy is insufficient.Here,we provide an updated overview of the function of autophagy as a regulator of neutrophils and discuss its clinical relevance to provide novel insight into potentially relevant treatment strategies. | Yao Yu Bingwei Sun | 2020 | Burns & Trauma2020，8，1： | 5 |
| 2 | Neutrophil-derived heparin binding protein triggers vascular leakage and synergizes with myeloperoxidase at the early stage of severe burns(With video)显示文摘Background:Burn shock caused by vascular leakage is one of the main causes of high mortality in severe burn injury.However,the pathophysiological mechanism of vascular leakage is still unclear.The purpose of this study was to explore the molecular mechanism of vascular leakage in the early stage of severe burn and provide a new target for the treatment of severe burns.Methods:Neutrophils were isolated from human peripheral blood by magnetic beads sorting.ELISA was used to detect neutrophil-derived granule proteins and glycocalyx injury products in plasma.The vascular leakage and neutrophil movement were assessed by in vivo laser confocal imaging in mice,and high-quality video were provided.Adhesion-related molecules were investigated by qRT-PCR.The damage to glycocalyx of mice vascular endothelial cellswas observed by transmission electron microscope and scanning electron microscope.Proteomic analysis,flow cytometry and immunofluorescence were used to further study the relationship between human peripheral blood neutrophil-derived hypochlorite(HOCl)and CD44 of human vascular endothelial cells.Results:In this study,we found that rapidly increasing activated neutrophils secrete heparin binding protein(HBP)andmyeloperoxidase(MPO)after severe burn injury.Increased HBP triggers vascular leakage with synergy of MPO,results in systemic edema and burn shock.Furthermore,we found that the MPO catalytic product HOCl but not MPO triggers CD44 extracellular domain shedding from vascular endothelial cells to damage the glycocalyx.Damage to the glycocalyx results in firm adhesion of neutrophils and increases vascular leakage.However,MPO inhibitors partially protect the glycocalyx of vascular endothelial cells.The combination of HBP and MPO inhibitors markedly reduces vascular leakage and systemic edema in the early stage of severe burns.Conclusions:Taken together,these data reveal that neutrophil-derived HBP and MPO play an important synergies role in triggering vascular leakage at the early stage of severe burns.Targeted intervention in these two biomolecules may introduce new strategies for helping to reduce large amount of fluid loss and subsequent burn shock. | Lu Liu Yiming Shao Yixuan Zhang Yunxi Yang Jiamin Huang Linbin Li Ran Sun Yuying Zhou Yicheng Su Bingwei Sun | 2021 | Burns & Trauma2021，9，1： | 3 |
| 3 | Neutrophil extracellular traps contribute to myofibroblast differentiation and scar hyperplasia through the Toll-like receptor 9/nuclear factor Kappa-B/interleukin-6 pathway显示文摘Background:Inflammation is an important factor in pathological scarring.The role of neutrophils,one of the most important inflammatory cells,in scar hyperplasia remains unclear.The purpose of this article is to study the correlation between neutrophil extracellular traps(NETs)and scar hyperplasia and identify a new target for inhibiting scar hyperplasia.Methods:Neutrophils were isolated from human peripheral blood by magnetic-bead sorting.NETs in plasma and scars were detected by enzyme-linked immunosorbent assays(ELISAs),immunofluorescence and flow cytometry.Immunohistochemistry was used to assess neutrophil(CD66B)infiltration in hypertrophic scars.To observe the entry of NETs into fibroblasts we used immunofluorescence and flow cytometry.Results:We found that peripheral blood neutrophils in patients with hypertrophic scars were more likely to form NETs(p<0.05).Hypertrophic scars showed greater infiltration with neutrophils and NETs(p<0.05).NETs activate fibroblasts in vitro to promote their differentiation and migration.Inhibition of NETs with cytochalasin in wounds reduced the hyperplasia of scars in mice.We induced neutrophils to generate NETs with different stimuli in vitro and detected the proteins carried by NETs.We did not find an increase in the expression of common scarring factors[interleukin(IL)-17 and transforming growth factor-β(TGF-β),p>0.05].However,inhibiting the production of NETs or degrading DNA reduced the differentiation of fibroblasts intomyofibroblasts.In vitro,NETs were found to be mediated by Toll-like receptor 9(TLR-9)in fibroblasts and further phosphorylated nuclear factor Kappa-B(NF-κB).We found that IL-6,which is downstream of NF-κB,was increased in fibroblasts.Additionally,IL-6 uses autocrine and paracrine signaling to promote differentiation and secretion.Conclusions:Our experiments found that NETs activate fibroblasts through the TLR-9/NF-κB/IL-6 pathway,thereby providing a new target for regulating hypertrophic scars. | Yiming Shao Zaiwen Guo Yunxi Yang Lu Liu Jiamin Huang Yi Chen Linbin Li Bingwei Sun | 2022 | Burns & Trauma2022，10，1： | 2 |
| 4 | Preconditioning of Carbon monoxide releasing molecule-derived CO attenuates LPS-induced activation of HUVEC 显示文摘 | Sun Bingwei Zou Xiangqian Chen Yueling | 2008 | Int J Biol Sci2008，4，5： | 1 |
| 5 | Role of CO-Releasing Molecules Liberated CO in Attenuating Leukocytes Sequestration and Inflammatory Responses in the Lung oiThermally Injured Mice 显示文摘 | Bingwei Sun Hui Sun Chang Liu | 2007 | J Surg Res2007，139，1： | 1 |
| 6 | Role of CO-releasing molecules liberated CO in attenuating leukocytes sequestration and inflammatory responses in the lung of thermally injured mice显示文摘 | Bingwei Sun Hui Sun Chang Liu | 2007 | J Surg Res2007，139，1： | 1 |
| 7 | Population turnover promotes fungal stability in a semi-arid grassland under precipitation shifts显示文摘土壤中细菌和真菌的稳定性在维持土壤生态系统功能方面起着重要作用,环境条件的改变直接影响细菌和真菌的组成与结构。已有研究表明,土壤真菌群落稳定性对降水变化响应的敏感性比细菌低,但其内在机制还不清楚。在内蒙古典型草原建立3年的增减降雨实验平台,设置5个降水梯度,包括分别增加和减少30%和60%的降水量以及对照,比较控制不同的降水水平对土壤细菌和真菌多样性的影响,包括α多样性,β多样性和细菌/真菌群落组成的变化。本研究开发了一个概念模型来反映不同降水条件下土壤细菌和真菌的稳定性特征,其中模型山谷的深度表示微生物抵抗力(Resistance),谷的宽度代表生态弹性(Ecological Resilience)。结果表明,增加和减少60%的降水量均显著降低了细菌的丰富度,同时显著增加了细菌均匀度,但对真菌的丰富度和均匀度没有显著的影响。降水对细菌α多样性的影响高于真菌,说明细菌对水分胁迫的敏感性大于真菌。而真菌群落的周转比细菌快,包括组成变化(Composition Variation),多样性指数和变异系数(Coefficient Variation),反映了真菌群落具有较高的群落可变性,使得降水变化对真菌群落的影响较小。概念模型中两种相反的情景表示细菌和真菌对降水变化不同的响应模式:真菌群落对水分胁迫响应不敏感,可以用宽谷中的一个球来表示,球虽然在较大范围内往复摆动,但仍接近稳定状态;而细菌群落对水分响应敏感,即稳定性低,可以表示为一个球在较窄的谷里远离平衡态的位置摆动。基于本研究结果,半干旱草原真菌群落比细菌群落具有更高的稳定性,该结论对于量化群落稳定性特征具有重要意义。 | Nannan Wang Lei Li Bingwei Zhang Shiping Chen Wei Sun Yukun Luo Kuanhu Dong Xingguo Han Jianhui Huang Xiaofeng Xu Changhui Wang | 2020 | Journal of Plant Ecology2020，13，4： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员