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Bifidobacteria DNA Induces Murine Macrophages Activation in vitro

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Cellular & Molecular Immunology 2005年第6期2卷 473-478页

作者： Yalin Li xun qu Hua Yang Li Kang Yingping Xu Bo Bai Wengang Song Department of Immunology Taishan Medical College Taian Shandong 271000 China Institute of Basic Medicine Qi Lu hospital of Shandong University Jinan 250012 China

Previous studies have shown that oligodeoxynucleotides containing unmethylated CpG motifs were used as adjuvants for immunoregulation and immune response. This study was to explore the activation effects of Bifidobacteria DNA containing unmethylated CpG motifs （CpG DNA） on murine macrophage J774A.1 cells. The genomic DNA of Bifidobacteria was extracted and purified, and the methylation degree of CpG motifs was tested. The phagocytic ability of the macrophages was detected by flow cytometry. The cytokines （IL-1β, IL-6, IL-12p40 and TNF-α） levels in the culture supernatants of Bifidobacteria DNA treated J774A.1 cells were assayed by ELISA. The content of nitric oxide （NO） was detected by Griess reagent. After treated with Bifidobacteria DNA for 24h, Nile Red stain increased in J774A.1 macrophage, which suggested that the lipid metabolism increased in the macrophages. The phagocytic ability and levels of NO and cytokines of IL-1β, IL-6, IL-12p40 and TNF-α were significantly higher than PBS group and CT DNA group. The results indicated that Bifidobacteria DNA could activate murine macrophages J774A.1, which could provide scientific basis for the research and application of microorganism DNA preparation. Cellular ＆ Molecular Immunology. 2005;2（6）：473-478.

关键词： Bifidobacteria DNA murine J774A. 1 macrophage phagocytic ability cytokine nitric oxide

Human trophoblast cells induced MDSCs from peripheral blood CD14＋ myelomonocytic cells via elevated levels of CCL2

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Cellular & Molecular Immunology 2016年第5期13卷 615-627页

作者： Yun Zhang Daiwei qu Jintang Sun Lei Zhao Qingjie Wang Qianqian Shao Beihua Kong xun qu Institute of Basic Medical Sciences Qilu Hospital Shandong University Jinan 250012 Shandong People's Republic of China Institute of Stomatology Qilu Hospital Shandong University Jinan 250012 Shandong People's Republic of China Department of Gynaecology and Obstetrics Qilu Hospital of Shandong University Jinan 250012 Shandong People's Republic of China The Key Laboratory of Cardiovascular Remodelling and Function Research Chinese Ministry of Education and Chinese Ministry of Health Qilu Hospital Shandong University Jinan 250012 Shandong People's Republic of China

Successful human pregnancy requires the maternal immune system to recognize and tolerate the semi-allogeneic fetus. Myeloid-derived suppressor cells （MDSCs）, which are capable of inhibiting T-cell responses, are highly increased in the early stages of pregnancy. Although recent reports indicate a role for MDSCs in fetal-maternal tolerance, little is known about the expansion of MDSCs during pregnancy. In the present study, we demonstrated that the trophoblast cell line HTR8/SVneo could instruct peripheral CD14＋ myelomonocytic cells toward a novel subpopulation of MDSCs, denoted as CD 14 ＋ H LA-DR-/=~w cells, with suppressive activity and increased expression of I DO 1, ARG- 1, a nd COX2. After interaction with HTR8/SVneo cells, CD14＋ myelomonocytic cells secrete high levels of CCL2, promoting the expression of signal transducer and activator of transcription 3. We utilized a neutralizing monoclonal antibody to reveal the prominent role of CCL2 in the induction of CD14＋HLA-DR-/low MDSCs. In combination, the results of the present study support a novel role for the cross-talk between the trophoblast cell line HTR8/SVneo and maternal CD14＋ myelomonocytic cells in initiating MDSCs induction, prompting a tolerogenic immune response to ensure a successful pregnancy.

关键词： CCL2 MDSCs tolerance in pregnancy trophoblast cells

Hypoxia induces T-cell apoptosis by inhibiting chemokine C receptor 7 expression:the role of adenosine receptor A2

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Cellular & Molecular Immunology 2010年第1期7卷 77-82页

作者： Jintang Sun Yan Zhang Meixiang Yang Yun Zhang Qi Xie Zewu Li Zhaogang Dong Yongmei Yang Biping Deng Alei Feng Weixu Hu Haiting Mao xun qu Institute of Basic Medical Sciences Qilu Hospital of Shandong UniversityJinanChina Shandong Center for Disease Control and Prevention JinanChina

Hypoxia is a major characteristic of the tumor microenvironment,and its effects on immune cells are proposed to be important factors for the process of tumor immune *** has been reported that hypoxia affects the function of dendritic cells and the antitumor function of T *** we discuss the effects of hypoxia on T-cell *** results showed that hypoxia induced apoptosis of T *** and adenosine receptors(AR)are important to the hypoxia-related signaling *** AR agonists and antagonists,we demonstrated that hypoxia-induced apoptosis of T cells was mediated by A^(2a)and A^(2b)***,we are the first,to our knowledge,to report that hypoxia significantly inhibited the expression of chemokine C receptor 7(CCR7)of T cells via the A^(2)R signal pathway,perhaps representing a mechanism of hypoxia-induced apoptosis of T ***,our research demonstrated that hypoxia induces T-cell apoptosis by the A^(2)R signaling pathway partly by suppressing *** the A^(2)R signaling pathway and/or activation of CCR7 can increase the anti-apoptosis function of T cells and may become a new strategy to improve antitumor potential.

关键词： adenosine receptor apoptosis CCR7 T cells

出版深度融合发展下的新编辑力“五力”探究——以广东省出版集团为例

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出版发行研究 2023年第12期 48-53页

作者：渠汛广东教育出版社

“编辑力”是编辑学的重要范畴,研究编辑力在新的出版生态与产业链中的内涵和要素,对编辑主体及出版企业的生产活动大有裨益。本文说明了出版深度融合发展的时代特征,系统阐述了编辑力的历史概念及讨论范畴,并以广东省出版集团为例,提... 详细信息

“编辑力”是编辑学的重要范畴,研究编辑力在新的出版生态与产业链中的内涵和要素,对编辑主体及出版企业的生产活动大有裨益。本文说明了出版深度融合发展的时代特征,系统阐述了编辑力的历史概念及讨论范畴,并以广东省出版集团为例,提出了在出版深度融合发展背景下,编辑出版活动应体现的新编辑力“五力”,即基于强化内容精品建设的资源整合力、基于优化内容呈现方式的全媒传播力、基于深化科技创新赋能的技术应用力、基于细化项目运营管理的产品经营力、基于活化文化产业融合的协同创新力,以期帮助编辑个人和出版企业更好地投入高质量出版实践,为出版强国建设贡献力量。

关键词：出版深度融合编辑力高质量出版出版强国

TECTONIC TRANSFER ON THE EASTERN EDGE OF PAMIR

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地学前缘 2000年第S1期7卷 88-89页

作者： Li Xiangdong, qu xun(Institute of Geology and Mineral Resources, Bureau of Geology and Mineral Resources of Xinjiang Uygur Autonomous Region, Urumqi 830000, China)

Deformation during the uplift of Pamir Since the Himalayan movement, the Punjab block of Indian plate has intruded into the interior of Eurasian plate, produced a protrusive Pamir knot in eastern Tethys. The Pamir knot is where crustal shortening is most intensive in Tethys. After India\|Eurasia collision, giant relief resulted from fast uplifting of Karakorum due to the convergence and underplating in northern and southern margins of Karakorum, the uplifting rates changed with times, and thrusting would be one of the most important factors controlling the uplifting. At the same time, large scale strike\|slip faulting could produced large vertical offsets, so that the exhumation of the rocks from middle and lower crust has drawn much attention. The post\|collisional deformation and evolution of Karakorum would involve the processes of continental escape, crustal shortening and thickening, and orogenic collapse in extensional regime. The thrusting started in late Jurassic and early Cretaceous, but two peaks occurred in late Cretaceous and Eocene, respectively. A large amount of klippen produced by thrusting from north to south have been discovered in the northern slope of the Kungai in front of Pamir. Molnar and Tapponnier noted that the mount of crustal shortening in Pamir would be up to 2000km in the past 40～45Ma, and Coward proposed that 300～400km shortening has happened only in southern Pamir to northern Pakistan. In western Pamir from Kabul of Afghanistan to quatta of Pakistan, the Chaman left\|lateral strike\|slip fault system extends 1000km long. Multiple structural superposition in eastern Pamir, due to the effects of the uplifting of Qinghai\|Tibet plateau, resulted in complex deformation patterns.

关键词： tectonic transfer the eastern edge of Pamir

Endostatin enhances antitumor effect of tumor antigen-pulsed dendritic cell therapy in mouse xenograft model of lung carcinoma

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Chinese Journal of Cancer Research 2016年第4期28卷 452-460页

作者： ring Liang Xiaolin Liu Qi Xie Guoling Chen Xingyu Li Yanrui Jia Beibei Yin xun qu Yan Li Department of Oncology Qianfoshan HospitalShandong UniversityJinan 250014China Central Laboratory Qianfoshan HospitalShandong UniversityJinan 250014China Islet Cell Lab MedStar Georgetown University HospitalWashington DC 20007USA Institute of Basic Medical Sciences and Key Laboratory of Cardiovascular Proteomics of Shandong Province Qilu HospitalShandong UniversityJinan 250012China

Objective： To investigate the antitumor effect of endostatin combined with tumor antigen-pulsed dendritic cell （DC）-T cell therapy on lung cancer. Methods： Transplanted Lewis lung cancer （LLC） models of C57BL/6 mice were established by subcutaneous injection of LLC cells in left extremity axillary. Tumor antigen-pulsed DC-T cells from spleen cells and bone of mice were cultured in vitro. Tumor-bearing mice were randomly divided into three groups, including DC- T＋endostatin group, DC-T group, and phosphate-buffered saline （PBS） control group. Microvessel density （MVD） of tumor tissue in tumor-bearing mice was determined by immunohistochemistry （IHC）. The expressions of vascular endothelial growth factor （VEGF） and hypoxia-inducible factor-1α （HIF-1α） were determined by Western blotting and IHC staining. The proportions of CD8＋ T cells, mature dendritic cells （mDC）, tumor-associated macrophages [TAM （M1/M2）], and myeloid-derived suppressor cells （MDSC） in suspended cells of tumor tissue were determined by flow cytometry. The expressions of inter｜eukin （IL）-6, IL-10, IL-17, transforming growth factor-β（TGF-β） and interferon-γ （IFN-γ） in suspended cells of tumor tissue were detected by enzyme-linked immune sorbent assay （ELISA）. Results： DC-T cells combined with endostatin remarkably suppressed tumor growth. MVD of mice in DC- T＋endostatin group was significantly lower than that of the control group and DC-T monotherapy group. The expressions of VEGF, IL-6 and IL-17 in tumors were markedly decreased, but IFN-γ, and HIF-1α increased after treating with DC-T cells combined with endostatin, compared to control group and DC-T group. In the DC- T＋endostatin group, the proportions of MDSC and TAM （M2 type） were significantly decreased, mDC and TAM （Nil type） were up-regulated, and CD8＋ T cells were recruited to infiltrate tumors, in contrast to PBS control and DC-T monotherapy. DC-T cells combined with endostatin potently reduced the expressions of IL-6, IL-10, TGF-β and IL-1

关键词： Endostatin DC-T cells lung cancer cellular therapy tumor microenvironment

Mechanism and antiviral function of hypoxia-induced trophoblast autophagy

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Mechanism and antiviral function of hypoxia-induced trophobl...

Expression of BAFF in the trophoblast and decidua of normal early pregnant women and patients with recurrent spontaneous miscarriage

第十三届全国免疫学学术大会

作者： jintang sun Bingfeng Song Chao Ma Xuanxuan Jing Dan Ai xun qu Qilu Hospital of Shandong University

Objective: To investigate the molecular mechanism and potential antiviral function of hypoxia-induced autophagy of trophoblast cells at the maternal fetal ***: Trophoblast cell line HTR-8 was cultured under normoxia and hypoxia condition *** level was evaluated by electron microscope and by the expression of LC3B and ***-related PCR array was used to screen potential molecules regulated by *** inhibitor and siRNA was uesd to determine the regulatory role of PTEN in hypoxia-induced ***-seq was used to investigate potential function of hypoxia-induced ***: We found that hypoxia significantly induced HTR-8 ***-related PCR array showed that hypoxia significantly upregulated PTEN ***, hypoxia inhibits Akt/mTOR pathway through PTEN, and further promotes HTR-8 *** with autophagy inhibitor 3-MA up-regulated 1459 gene and down-regulated 1496 gene *** and KEGG analysis indicated that trophoblast autophagy was involved in the regulation of antiviral *** further showed that hypoxia regulated Poly I:C stimulated IFN-β1 via autophagy in ***: Our study revealed the regulatory role of PTEN in hypoxia-induced trophoblast autophagy, and firstly investigated potential antiviral role of hypoxia-induced trophoblast at maternal-fetal interface.

关键词： trophoblast autophagy hypoxia antiviral function

来源： cnki会议评论

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Chinese Medical Journal 2008年第4期121卷 309-315页

作者： GUO Wen-jing qu xun YANG Mei-xiang ZHANG Wei-dong LIANG Lu SHAO Qian-qian KONG Bei-hua Department of Obstetrics and Gynecology Qilu Hospital ShandongUniversity Jinan Shandong 250012 China Basic Research Institute of Clinic Medicine Qilu Hospital ShandongUniversity Jinan Shandong 250012 China Department of Obstetrics and Gynecology Second Hospital Shandong University Jinan Shandong 250012 China Department of Pathology Institute of Basic Medicine Shandong Academy of Medical Sciences Jinan Shandong 250012 China

Background BAFF, the B cell activation factor, is a member of the tumor necrosis factor （TNF） ligand family that binds to BCMA, TACI, and BAFF-R. Previous studies have shown that members of the TNF family are detected in human placental trophoblast cells, but the expression patterns of BAFF involved in human decidua and the differential expression of BAFF between normal pregnancy and miscarriage are still incompletely documented or unknown. This study was designed to investigate the expression of BAFF and BAFF-R in the trophoblast and decidua of normal early pregnant women and recurrent spontaneous abortion （RSA） patients.Methods Forty-five patients with RSA and 45 normal pregnant women were included in this study. By reverse transcriptase-polymerase chain reaction （RT-PCR）, Western blotting and immunohistochemical experiments, we explored the expression of BAFF and BAFF-R in the maternal-fetal interface of normal early pregnant women and RSA patients.Results Analysis by RT-PCR and Western blotting revealed that BAFF was detected in both trophoblast and decidua of all the samples, and the expression level was higher in the tissues of normal early pregnant women （P〈0.05） than that of recurrent spontaneous abortion patients under the same gestational weeks. Messages for BAFF-R were absent. Immunohistochemical experiments showed that expression of BAFF was cell-specific which was localized to villous cytotrophoblast and syncytiotrophoblast cells in trophoblast and to stromal cells in decidua. Whereas BAFF was prominent on the trophoblast and decidua of normal early pregnant women, it was decreased in the tissues of RSA patients.Conclusions BAFF might steer maternal leukocytes away from a harmful immune response and toward a favorable one and play a potentially vital role for successful pregnancy.

关键词： B lymphocyte stimulator recurrent spontaneous abortion maternal-fetal immunology

Response gene to complement 32 （RGC-32） expression on M2-polarized and tumor-associated macrophages is M-CSF-dependent and enhanced by tumor-derived IL-4

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Cellular & Molecular Immunology 2015年第6期12卷 692-699页

作者： Peng Zhao Daiqing Gao Qingjie Wang Bingfeng Song Qianqian Shao Jintang Sun Chunyan Ji Xingang Li Peng Li xun qu Institute of Basic Medical Sciences Qilu Hospital Shandong University Jinan China Biotherapy Center Qingdao Central Hospital the Second Affiliated Hospital Qingdao University Medical College Qingdao China Neurosurgery Qilu Hospital of Shandong University Jinan China

Response gene to complement 32 （RGC-32） is a cell cycle regulator involved in the proliferation, differentiation and migration of cells and has also been implicated in angiogenesis. Here we show that RGC-32 expression in macrophages is induced by IL-4 and reduced by LPS, indicating a link between RGC-32 expression and M2 polarization. We demonstrated that the increased expression of RGC-32 is characteristic of alternatively activated macrophages, in which this protein suppresses the production of pro-inflammatory cytokine IL-6 and promotes the production of the anti-inflammatory mediator TGF-β. Consistent with in vitro data, tumor-associated macrophages （TAMs） express high levels of RGC-32, and this expression is induced by tumor-derived ascitic fluid in an M-CSF- and/or IL-4-dependent manner. Collectively, these results establish RGC-32 as a marker for M2 macrophage polarization and indicate that this protein is a potential target for cancer immunotherapy, targeting tumor-associated macrophages.

关键词： macrophage polarization monocyte response gene to complement 32