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1. Pseudomonas aeruginosa promotes autophagy to suppress macrophage-mediated bacterial eradication | |||
Wenting Qu,Yongjian Wu,Dandan Li,Yi Wang,Minhao Wu | |||
Basic Medicine 26 May 2016 | |||
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Abstract:Objectives: To explore the role of autophagy on macrophage-mediated phagocytosis and intracellular killing of Pseudomonas aeruginosa (PA), a common extracellular bacterium which often causes various opportunistic infections. Methods: Macrophages were infected with PA or stimulated with zymosan bioparticles. Autophagy was tested by fluorescent microscopy and Western blot for LC3. Phagocytosis and killing efficiency were assessed by plate count assay, flow cytometry or immunofluorescent staining. Phagocytic receptor expression, ROS generation and NO production were examined by PCR, flow cytometry and Griess reaction, respectively. Results: PA infection induced autophagy activation in both mouse and human macrophages. Induction of autophagy by rapamycin or starvation significantly inhibited PA internalization by downregulating phagocytosis receptor expression, and suppressed intracellular killing of PA via reducing ROS and NO production in macrophages. While knockdown of autophagy molecules ATG7 or Beclin1 enhanced macrophage-mediated phagocytosis and intracellular killing of PA. Conclusions: Our study suggested that PA promotes autophagy to suppress macrophage-mediated bacterial phagocytosis and intracellular killing. These insights demonstrated a novel immune evasion mechanism employed by PA, which may provide potential therapeutic strategies of PA infectious diseases. | |||
TO cite this article:Wenting Qu,Yongjian Wu,Dandan Li, et al. Pseudomonas aeruginosa promotes autophagy to suppress macrophage-mediated bacterial eradication[OL].[26 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4692951 |
2. MicroRNAs : New Regulators of IL-22 | |||
Zhou Lu,Ronghua Liu,Enyu Huang,Yiwei Chu | |||
Basic Medicine 16 May 2016 | |||
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Abstract:Interleukin-22 (IL-22) is a cytokine which belongs to IL-10 family. It is produced by T helper 22 (Th22) cells, T helper 1 (Th1) cells, T helper 17 (Th17) cells, natural killer 22 (NK22) cells, natural killer T (NKT) cells, innate lymphoid cells (ILCs) and γδ T cells. IL-22 exerts its functions via binding to a heterodimeric transmembrane receptor complex consisting of IL-22R1 and IL-10R2. IL-22 mainly contributes to tissue repair and host defense. Transcription factors such as retinoid orphan receptor γt (RORγt) and signal transducer and activator of transcription 3 (STAT3) have been reported to play important roles in the regulation of IL-22. Recently, several studies have reported that microRNAs (miRNAs) emerged as powerful regulators of interleukins including IL-22. Here, we introduce the regulators of IL-22, particularly emphasized the miRNAs. ????? | |||
TO cite this article:Zhou Lu,Ronghua Liu,Enyu Huang, et al. MicroRNAs : New Regulators of IL-22[OL].[16 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4689180 |
3. Interleukin-6 Regulates Voltage-Gated Sodium channels in a Time- and Dose-Dependent Manner in Rat Cortical Neurons | |||
SHENG Jiangtao,GAO fenfei,CHEN Weiqiang,DENG Lijuan,GUO Jingfang,WANG Gefei,DAI Jianping,HUANG Zhengyi,SHI Ganggang,LI Kangsheng | |||
Basic Medicine 10 January 2013 | |||
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Abstract:The cytokine interleukin-6 (IL-6) is expressed at elevated levels within the CNS in many neurological disorders and may contribute to the histopathological, pathophysiological, and cognitive deficits associated with such disorders. However, the effects of chronic IL-6 exposure on neuronal function in the CNS are largely unknown. A voltage-gated Na+ channel is essential for the excitability and electrical properties of neurons. Therefore, using patch-clamp recording we investigated the effects of chronic IL-6 exposure on voltage-gated Na+ channels. Our results showed that IL-6 suppressed Na+ currents through its receptor in a time- and dose-dependent manner, but did not alter the voltage-dependent activation and inactivation. The spike amplitude was also inhibited by IL-6 in the doses that decreased Na+ currents. The present data reveals chronic exposure to elevated levels of IL-6, such as occurs in various neurological diseases, produces inhibition in the voltage-gated Na+ channels without the alterations in single-channel characteristics. The results support the hypothesis that chronic IL-6 exposure can disrupt normal CNS function and thereby contribute to the pathophysiology associated with many neurological diseases. | |||
TO cite this article:SHENG Jiangtao,GAO fenfei,CHEN Weiqiang, et al. Interleukin-6 Regulates Voltage-Gated Sodium channels in a Time- and Dose-Dependent Manner in Rat Cortical Neurons[OL].[10 January 2013] http://en.paper.edu.cn/en_releasepaper/content/4513574 |
4. Induction of cytopathic effect and cytokines in coxsackievirus B3-infected murine astrocytes | |||
ZENG Jun,WANG Gefei,LI Weizhong,CHEN Xiaoxuan,XIN Gang,ZHANG Dangui,JIANG Zhiwu,LI Kangsheng | |||
Basic Medicine 09 January 2013 | |||
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Abstract:Coxsackievirus commonly infects children and occasionally causes severe meningitis and/or encephalitis in the newborn. The underlying mechanism(s) behind the central nervous system pathology is poorly defined. It is hypothesized that astrocytes may be involved in inflammatory response induced by CVB3 infection. Here we discuss this hypothesis in the context of CVB3 infection and associated inflammatory response in primary mouse astrocytes. CVB3 infected and replicated in astrocytes, with release of infectious virus particles. CVB3 induced cytopathic effect (CPE) and production of proinflammatory cytokines IL-1β, TNF-α, IL-6, and chemokine CXCL10 from astrocytes. These data suggest that direct astrocyte damage and cytokines induction could be a mechanism of virus-induced neuropathology. | |||
TO cite this article:ZENG Jun,WANG Gefei,LI Weizhong, et al. Induction of cytopathic effect and cytokines in coxsackievirus B3-infected murine astrocytes[OL].[ 9 January 2013] http://en.paper.edu.cn/en_releasepaper/content/4513097 |
5. Macrophang inflammatory protein 3 beta promotes survival in rat primary cortical neurons and PC12 cells | |||
MA Jun,QIAN Xiying,JIN Lide,FANG Shaolong,FU Guoping,CAO Yi,XU Wei,CAO Xia | |||
Basic Medicine 10 December 2012 | |||
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Abstract:Background We have previously reported that CCR7 may be neuroprotective in the central nervous system. This study aimed to investigate whether macrophage inflammatory protein 3 beta (MIP-3 beta /CCL19), which is the ligand for CCR7, could promote survival in primary neurons and PC12 cells in vitro. Results We found that within the concentration range of 50 to 200 ng/ml, MIP-3 beta promoted survival in serum-deprived rat primary cortical neurons as well as reduced serum deprivation-induced Bim expression. However, primary cortical neurons were less viable at higher concentrations of MIP-3 beta (≥300 ng/ml). To investigate whether MIP-3 beta acts through its receptor, CCR7, the pEGFP-N1-CCR7 expression vector was constructed and transfected into PC12 cells. We found that MIP-3 beta enhanced survival of PC12 cells that were transfected with pEGFP-N1-CCR7 in serum-free media. In these transfected PC12 cells, MIP-3 beta increased Akt phosphorylation levels at 15 and 60 min this effect was effectively blocked by wortmannin, a specific PI3K inhibitor. ConclusionsThese data suggest that MIP-3 beta promotes survival in serum-deprived rat primary cortical neurons through its receptor, CCR7, and acts as a neurotrophic factor in PC12 cells, most likely via the PI3K/Akt signaling pathway. | |||
TO cite this article:MA Jun,QIAN Xiying,JIN Lide, et al. Macrophang inflammatory protein 3 beta promotes survival in rat primary cortical neurons and PC12 cells[OL].[10 December 2012] http://en.paper.edu.cn/en_releasepaper/content/4500497 |
6. Role of γ-Interferon in Induction of Foxp3 and Conversion of CD4+CD25- T cells to CD4+ Regulatory T Cells | |||
Wang Zhaojun,Hong Jian,Sun Wei,Xu Guangwu,Li Ningli,Chen Xi,Liu Ailian,Xu Lingyun,Sun Bing,Zang Jingwu | |||
Basic Medicine 16 January 2009 | |||
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Abstract:γ−Interferon (γ−IFN) is an important Th1 pro-inflammatory cytokine and has a paradoxical effect on experimental autoimmune encephalomyelitis (EAE) in which the disease susceptibility is unexpectedly heightened in γ−IFN deficient mice. In this study, we provided new evidence indicating that γ−IFN was critically required for the conversion of CD4+CD25- T cells to CD4+ regulatory T cells during EAE. The study showed that the added severity of EAE in γ−IFN knockout mice was directly associated with altered encephalitogenic T cell responses, which correlated with reduced frequency and function of CD4+CD25+Foxp3+ regulatory T cells when compared to wild-type mice. It was demonstrated in both human and mouse systems that in vitro γ−IFN treatment of CD4+CD25- T cells converted to CD4+ regulatory T cells characterized by increased expression of Foxp3 and enhanced regulatory function. Mouse CD4+CD25- T cells, when treated in vitro with γ−IFN, acquired marked regulatory properties as evidenced by suppression of EAE by adoptive transfer. The findings have important implications for the understanding of the complex role of γ−IFN in both induction and self regulation of inflammatory processes. | |||
TO cite this article:Wang Zhaojun,Hong Jian,Sun Wei, et al. Role of γ-Interferon in Induction of Foxp3 and Conversion of CD4+CD25- T cells to CD4+ Regulatory T Cells[OL].[16 January 2009] http://en.paper.edu.cn/en_releasepaper/content/27933 |
7. 4-1BBL reverse signaling potently induces Dendritic Cells development from human monocytes | |||
Songguang Ju,Songwen Ju,Xueguang Zhang | |||
Basic Medicine 08 January 2009 | |||
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Abstract:Dendritic cells (DCs) are responsible for the initiation of immune responses. Our study demonstrates a new pathway for generating a large quantity of stimulatory monocyte derived DCs (Mo-DCs) from human monocytes using anti-4-1BB Ligand (4-1BBL) mAb to trigger reverse signaling. The anti-4-1BBL-driven-Mo-DCs (DCsα-4-1BBL) not only express higher levels of CD86, CD83 and HLA-DR, when compared to the Mo-DCs matured by TNF-α, they also exhibit a unique phenotype that expresses lower levels of PD-L1. High levels of GM-CSF, M-CSF, and Flt3 Ligand(FL) were found in the anti-4-1BBL-differentiation culture. Neutralizing M-CSF, GM-CSF, and FL inhibited Mo-DC proliferation stimulated by anti-4-1BBL mAb, suggesting that M-CSF, GM-CSF, and FL are involved in cell proliferation stimulated by anti-4-1BBL. Further analysis of the DCsα-4-1BBL showed increased secretion of Th1-type cytokines IL-12 and IFN-γ, and decreased secretion of IL-10. DCsα-4-1BBL induced much stronger proliferative responses in the MLR assay when compared with DCs derived by GM-CSF. Moreover, DCsα-4-1BBL preferentially induced Th1 responses. We have further demonstrated that anti-4-1BBL antibody stimulated nuclear translocation of NF-κB from the cytoplasm in monocytes, suggesting reverse signaling by 4-1BBL is likely responsible for mediating DCs differentiation. Collectively, we have found that reverse signaling of 4-1BBL promotes the differentiation of potent Th1-inducing DCs from human monocytes. | |||
TO cite this article:Songguang Ju,Songwen Ju,Xueguang Zhang. 4-1BBL reverse signaling potently induces Dendritic Cells development from human monocytes[J]. |
8. Hyperactivated uterine NK cells contribute more for the regulation of murine pregnancy | |||
Zhang Jianhong,Sun Rui,Wei Haiming,Wu Dongmei,Tian Zhigang | |||
Basic Medicine 14 November 2006 | |||
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Abstract:To understand the response of murine uterine natural killer (uNK) cells to Toll-like receptor (TLR) 3 agonist at the early stage of gestation, CBA×DBA/2 mice were intraperitoneally (i.p.) injected with polyinosinic-polycytidylic acid (poly I:C), the specific TLR-3 agonist, at dose of 10 μg/g·BW or PBS at gestation day (gd) 6.5. The percentage of intracellular TNF-α+ or IFN-γ+ uNK (DX5+CD3-) cells in the implantation sites of CBA×DBA/2 matings were significantly increased 24 hours after poly I:C injection. Surprisingly, poly I:C treatment significantly decreased the total number of uNK cells (either DX5+CD3- or DBA+) at fetal maternal surface, but had no influence on local NKT cells, T cells and DCs. This investigation will help to explain the central role for hyperactivated uNK cells in the progress of mice pregnancy. | |||
TO cite this article:Zhang Jianhong,Sun Rui,Wei Haiming, et al. Hyperactivated uterine NK cells contribute more for the regulation of murine pregnancy[OL].[14 November 2006] http://en.paper.edu.cn/en_releasepaper/content/9532 |
9. Decidual TLR signal response associated with TNF-α regulate the uterine spiral artery transformation of CBA×DBA/2 mice | |||
Zhang Jianhong,Sun Rui,Wei Haiming,Wu Dongmei,Tian Zhigang | |||
Basic Medicine 14 November 2006 | |||
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Abstract:The objective of this study was to examine the expression of Toll-like receptor (TLR) 3 at maternal fetal interface and determine whether exposure to the TLR3 agonist would induce innate immune response and trigger pregnancy loss. To address this, abortion-prone male DBA/2J mated-CBA/J female mice were given polyinosinic-polycytidylic acid (poly I:C, 10 μg/g·body weight, i.p.) or PBS at gestation day (gd) 6.5. All implantation sites appeared viable at gd 7.5 when endometrium was dissected for immunohistological examination. It was noted that poly I:C treatment increased fetal losses to 40.2±1.7% at midgestation stage, compared with control animals (11.0±3.0%). It was also observed that the ratio of vessel area to lumen area significantly increased at gd 10.5 and gd 12.5 after poly I:C treatment, indicating that the spiral arterial (SA) modification was impaired. Meanwhile, twenty-four hours after poly I:C injection, the expression of TLR3 dramatically elevated within decidua basalis (DB), and content of the endometrial TNF-α increased 2.7 fold but IFN-γ remained unchanged in homogenized endometrium. These results suggested that enhanced TNF-α expression in endometrial stroma may play a critical role in inflammatory factor production and the impairment of uterine spiral artery remodeling in the pregnancy failure of CBA×DBA/2 mating | |||
TO cite this article:Zhang Jianhong,Sun Rui,Wei Haiming, et al. Decidual TLR signal response associated with TNF-α regulate the uterine spiral artery transformation of CBA×DBA/2 mice[OL].[14 November 2006] http://en.paper.edu.cn/en_releasepaper/content/9512 |
10. Neonatal Murine Keratinocytes Split Express CD80/CD86 upon Culture | |||
LeiJianjun,ChengJingqiu,LiYouping,LiShengfu,ZhangLi,KeNengwen | |||
Basic Medicine 28 December 2005 | |||
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Abstract:It was previously thought that keratinocytes did not express the CD80 and CD86 which provide the most important costimulatory signals for the antigen-specific T-cell activation.The cultured keratinocytes allografts were initially accepted,but eventually,allgrafted donor cells were gradually replaced by recipient cells.The precise mechanisms are not very clear.In this study,neonatal murine keratinocytes were cultured for 7 days,the results of flowcytometry and confocal microscopy showed that CD80 could be detected on keratinocytes,whileCD86 could not be detected all the time.RT-PCR analysis confirmed this result.The expression level of the CD80 mRNA amplified significantly from day1 to day 7,as expression of the control B-actin,but CD86 was not detected.Mixed Lymphocyte Reaction(MLR) showed that keratinocytes cultured with 10% serum for 7d stimulated effectively allogeneic rather than syngeneic T cell proliferation.This study demonstrated for the first time that co-stimulatory molecule CD80 can be expressed onkeratinocytes invitro.These data provided an alternative explanation for the ultimate rejection of allogeneic keratinocytes in which keratinocytes act as antigen-presenting cells. | |||
TO cite this article:LeiJianjun,ChengJingqiu,LiYouping, et al. Neonatal Murine Keratinocytes Split Express CD80/CD86 upon Culture[OL].[28 December 2005] http://en.paper.edu.cn/en_releasepaper/content/4704 |
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