检索结果-内蒙古大学图书馆

Ability of Ni-containing biomedical alloys to activate monocytes and endothelial cells in vitro

JOURNAL OF BIOMEDICAL MATERIALS RESEARCH 1999年第3期45卷 251-257页

作者： Wataha, JC Lockwood, PE Marek, M Ghazi, M Med Coll Georgia Sch Dent Dept Oral Rehabil Augusta GA 30912 USA Georgia Inst Technol Atlanta GA 30332 USA Georgia State Univ Atlanta GA 30303 USA

Nickel-containing alloys commonly are used in medical and dental applications that place them into longterm contact with soft: tissues. The release of Ni ions from these alloys is disturbing because of the toxic, immunologic, and carcinogenic effects that have been documented for some Ni compounds. In particular, Ni ions in solution recently have been shown to cause expression of inflammatory mediators, such as interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and intercellular adhesion molecules (ICAMs) from keratinocytes, monocytes, and endothelial cells. However, the ability of the solid alloys themselves to induce these inflammatory effects has not been demonstrated. An in vitro system was used to determine if Ni-containing biomedical alloys could cause secretion of either IL-1 beta or TNF-alpha from monocytes or expression of ICAMs on endothelial cells. Pure nickel, titanium, and three biomedical alloys-18-8 stainless steel, NiTi, and Rexillium III-were evaluated. First, it was determined whether or not the alloys or pure metals could cause cytotoxicity to THP-1 human monocytes or human microvascular endothelial cells (HMVECs) by measuring the succinic dehydrogenase (SDH) activity of the cells. Then, using identical conditions of exposure, the secretion of IL-1 beta or TNP-alpha from monocytes or ICAM-1 expression on the HMVECs was determined. Only pure nickel suppressed (by 48% compared to Teflon controls) the SDH activity of the HMVECs or THT-1 monocytes. No alloy or metal caused the HMVECs to express ICAM-1, but the NiTi alloy caused a significant (ANOVA/Tukey) secretion of IL-1 beta from the THP-1 monocytes. Secretion of TNF-alpha induced by NiTi was detectable but not statistically significant. The levels of IL-1 beta secretion from monocytes were sufficient to induce ICAM-1 expression on HMVECs. The release of Ni from the NiTi was a logical suspect in causing the IL-1 beta secretion by monocytes, but its role was not confirmed since

关键词：合金/毒性毛细血管/细胞学毛细血管/药物作用细胞存活/药物作用细胞培养的内皮血管/细胞学内皮血管/药物作用内皮血管/代谢胞间黏附分子1/生物合成白细胞介素1/代谢巨噬细胞活化/药物作用单核细胞/化学单核细胞/药物作用镍/分析镍/毒性琥珀酸脱氢酶/代谢钛/毒性肿瘤坏死因子α/代谢人类

来源：评论

学校读者我要写书评

暂无评论

Regulation of arachidonic acid mobilization in lipopolysaccharide-activated P388D₁ macrophages by adenosine triphosphate

引用

JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第51期274卷 36764-36768页

作者： Balboa, MA Balsinde, J Johnson, CA Dennis, EA Univ Calif San Diego Dept Biochem & Chem La Jolla CA 92093 USA

Murine P388D, macrophages exhibit a delayed prostaglandin biosynthetic response when exposed to bacterial lipopolysaccharide (LPS) for prolonged periods of time that is dependent on induction of the genes coding for Group V secretory phospholipase A(2) and cyclooxygenase-2, We herein report that LPS-induced arachidonic acid (AA) metabolite release in P388D(1) macrophages is strongly attenuated by the P2X(7) purinergic receptor antagonists periodate-oxidized ATP and pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid, and this is accompanied by suppression of the expression of both Group V secretory phospholipase A(2) and cyclooxygenase-2, The effect appears to be specific for LPS, because the P2X(7) purinergic receptor antagonists do not affect P388D, cell stimulation by other stimuli such as platelet-activating factor or the Ca2+ ionophore A23187. Moreover, extracellular nucleotides are found to stimulate macrophage AA mobilization with a pharmacological profile that implicates the participation of the P2X(7) receptor and that is inhibited by periodate-oxidized ATP. Collectively these results demonstrate coupling of the P2X(7) receptor to the AA cascade in P388D, macrophages and implicate the participation of this type of receptor in LPS-induced AA mobilization.

关键词：腺苷三磷酸/代谢花生四烯酸/代谢白血病P388/代谢脂多糖类/药理学巨噬细胞活化/药物作用巨噬细胞/代谢信号传导肿瘤细胞培养的动物

来源：评论

学校读者我要写书评

暂无评论

Hck enhances the adherence of lipopolysaccharide-stimulated macrophages via Cbl and phosphatidylinositol 3-kinase

引用

JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第19期275卷 14615-14623页

作者： Scholz, G Cartledge, K Dunn, AR Royal Melbourne Hosp Ludwig Inst Canc Res Mol Biol Lab Melbourne Vic 3050 Australia

Src family tyrosine kinases have previously been proposed to mediate some of the biological effects of lipopolysaccharide on macrophages, Accordingly, we have sought to identify substrates of Src family kinases in lipopolysaccharide-stimulated macrophages. Stimulation of Bac1.2F5 macrophage cells with lipopolysaccharide was found to induce gradual and persistent tyrosine phosphorylation of Cbl in an Src family kinase-dependent manner. Immunoprecipitation experiments revealed that Cbl associates with Hck in Bac1.2F5 cells, while expression of an activated form of Hck in Bac1.2F5 cells induces tyrosine phosphorylation of Cbl in the absence of lipopolysaccharide stimulation. The Src homology 3 domain of Hck can directly bind Cbl, and this interaction is important for phosphorylation of Chi. Association of the p85 subunit of phosphatidylinositol (PI) 3-kinase with Cbl is enhanced following lipopolysaccharide stimulation of Bac1.2F5 cells, and transient expression experiments indicate that phosphorylation of Cbl by Hck can facilitate the association of p85 with Cbl, Lipopolysaccharide treatment also stimulates the partial translocation of lick to the cytoskeleton of Bac1.2F5 cells. Notably, lipopolysaccharide enhances the adherence of Bac1.2F5 cells, an effect that is dependent on the activity of Src family kinases and PI 3-kinase. Thus, we postulate that Hck enhances the adherence of lipopolysaccharide-stimulated macrophages, at least in part, via Cbl and PI 3-kinase.

关键词：生物转运细胞黏附/生理学细胞系细胞骨架/代谢脂多糖类/药理学巨噬细胞活化/药物作用巨噬细胞/细胞学巨噬细胞/药物作用巨噬细胞/酶学巨噬细胞/代谢磷酸肌醇3-激酶类/代谢磷酰化蛋白酪氨酸激酶类/生理学原癌基因蛋白质类/代谢原癌基因蛋白质类/生理学原癌基因蛋白质c-cbl 原癌基因蛋白质c-hck 泛素蛋白连接酶类 src同源域

来源：评论

学校读者我要写书评

暂无评论

Glucocorticoid modulation of gp120-induced effects on calcium-dependent degenerative events in primary hippocampal and cortical cultures

引用

EXPERIMENTAL NEUROLOGY 1999年第1期158卷 164-170页

作者： Howard, SA Nakayama, AY Brooke, SM Sapolsky, RM Stanford Univ Dept Biol Sci Stanford CA 94305 USA

The HIV coat protein gp120 has been implicated in damaging the nervous system and may play a role ih AIDS-related dementia complex. The glycoprotein triggers the release of a glutamatergic agent from infected microglia and macrophages, causing NMDA receptor and calcium-dependent excitotoxic damage to neurons. We have previously shown that glucocorticoids, the adrenal steroids secreted during stress, worsen gp120 neurotoxicity and calcium mobilization in various brain regions. This study explores events down stream of gp120-induced calcium mobilization, specifically, generation of reactive oxygen species (ROS) and subsequent lipid peroxidation, destruction of the cytoskeleton through spectrin proteolysis, and the glucocorticoid modulation of these events in primary hippocampal cultures. We observe that 200 pM gp120 causes a significant accumulation of ROS, including superoxide, and of lipid peroxidation. Counter to our predictions, pretreatment with the glucocorticoid corticosterone (CORT) did not worsen the effects of gp120 on ROS accumulation, but did increase Lipid peroxidation. We also observed that neither gp120 alone nor gp120 plus CORT caused detectable proteolysis of the cytoskeletal protein spectrin, whose breakdown has been shown to be a damaging consequence of calcium excess in other models of necrotic neuronal injury. (C) 1999 Academic Press.

关键词：钙/代谢细胞培养技术大脑皮质/药物作用大脑皮质/病理学皮质酮/药理学糖皮质激素类/药理学 HIV包膜蛋白质gp120/药理学海马/药物作用海马/病理学脂质过氧化作用/药物作用巨噬细胞活化/药物作用巨噬细胞/药物作用小神经胶质细胞/药物作用神经变性/病理学神经元/药物作用神经元/病理学肽水解酶类/代谢活性氧/代谢受体 N-甲基-D-天冬氨酸/药物作用超氧化物类/代谢动物大鼠

来源：评论

学校读者我要写书评

暂无评论

Comparative analysis of CD137 and LPS effects on monocyte activation, survival, and proliferation

引用

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2000年第1期273卷 117-122页

作者： Langstein, J Becke, FM Söllner, L Krause, G Brockhoff, G Kreutz, M Andreesen, R Schwarz, H Univ Regensburg Dept Pathol D-93042 Regensburg Germany Univ Regensburg Dept Hematol D-93042 Regensburg Germany

CD137 (ILA/4-1BB), a member of the TNF receptor family, regulates activation, survival and proliferation of primary human monocytes, Here we compare the activities of lipopolysaccharide (LPS), a classical and potent monocyte activator to that of CD137. LPS is a more potent activator of monocytes, as evidenced by a stronger induction of the proinflammatory cytokine IL-8, However, CD137 could further increase maximal cytokine induction by LPS, which points to separate signaling pathways for LPS and CD137. Also, expression of myc was only induced by the combination of CD137 and LPS. Expression of macrophage colony-stimulating factor is induced more potently by CD137, but an additive effect is obtained by the combination of CD137 and LPS. Monocyte/macrophage survival and proliferation is only induced by CD137. LPS counteracts both activities of CD137 via activation induced cell death. While LPS has a role in activation of monocytes in innate immunity, the CD137 receptor/ligand system seems to deliver an activating signal to monocyte in acquired immunity. (C) 2000 Academic Press.

关键词：抗原 CD 抗原 CD137 细胞凋亡/药物作用细胞黏附/药物作用细胞分裂/药物作用细胞存活/药物作用细胞培养的基因表达调控/药物作用基因 myc/遗传学白细胞介素8/代谢脂多糖类/药理学巨噬细胞活化/药物作用巨噬细胞集落刺激因子/代谢单核细胞/细胞学单核细胞/药物作用单核细胞/免疫学单核细胞/代谢 RNA 信使/遗传学 RNA 信使/代谢受体神经生长因子类/拮抗剂和抑制剂受体神经生长因子类/代谢受体肿瘤坏死因子/拮抗剂和抑制剂受体肿瘤坏死因子/代谢重组融合蛋白质类/代谢信号传导/药物作用人类

来源：评论

学校读者我要写书评

暂无评论

The antiinflammatory drug sulfasalazine inhibits tumor necrosis factor α expression in macrophages by inducing apoptosis

引用

ARTHRITIS AND RHEUMATISM 2000年第9期43卷 1941-1950页

作者： Rodenburg, RJT Ganga, A van Lent, PLEM van de Putte, LBA van Venrooij, WJ Univ Nijmegen Dept Biochem NL-6500 HB Nijmegen Netherlands TNO Pharma Zeist Netherlands

Objective. Sulfasalazine (SSZ) is a commonly used drug in the treatment of inflammatory diseases such as rheumatoid arthritis and Crohn's disease. In both diseases, the proinflammatory cytokine tumor necrosis factor alpha (TNF alpha) plays a prominent role. In these studies, we investigated the mechanism by which SSZ inhibits TNF alpha expression in macrophages and macrophage-like cell lines. Methods. Monocyte-derived macrophages and several macrophage-like cell lines were exposed to SSZ in vitro, and the effect on TNF alpha expression was monitored by reverse transcriptase-polymerase chain reaction and Western blot analysis. In addition, the effects of SSZ in vivo were examined by intraperitoneally injecting mice with SSZ, after which peritoneal cells were harvested and examined using various staining methods. Results. Preincubation of macrophages with SSZ, but not with methotrexate, inhibited lipopolysaccharide (LPS)-induced TNF alpha expression. Inhibition of TNF alpha expression by SSZ coincided with the induction of apoptosis, as judged by the appearance of morphologic changes typical of apoptosis, such as nuclear condensation and fragmentation. Induction of apoptosis by SSZ was confirmed by TUNEL analysis and by the detection of cleaved U1-70K, a substrate of caspase 3. Intraperitoneal injections of SSZ in mice resulted in the induction of apoptosis of peritoneal cells within a few hours. SSZ-induced cleavage of the U1-70K protein was inhibited by Zn2+ and by specific inhibitors of caspases 3 and 8, but not caspases 1 and 9. Interestingly, the reduced expression of LPS-induced TNF alpha in the presence of SSZ was restored by inhibition of caspase 8. Conclusion. Inhibition of TNF alpha expression in macrophages by SSZ is due to the induction of apoptosis and involves the activation of caspase 8.

关键词：腺苷/药理学消炎药非甾类/药理学细胞凋亡/药物作用半胱氨酸天冬氨酸蛋白酶/拮抗剂和抑制剂细胞培养的半胱氨酸蛋白酶抑制剂/药理学巨噬细胞活化/药物作用巨噬细胞/细胞学巨噬细胞/代谢巨噬细胞腹膜/细胞学巨噬细胞腹膜/代谢甲氨蝶呤/药理学小鼠近交C57BL 柳氮磺胺吡啶/药理学肿瘤坏死因子α/拮抗剂和抑制剂肿瘤坏死因子α/生物合成动物人类小鼠

来源：评论

学校读者我要写书评

暂无评论

In vivo macrophage activation in chickens with Acemannan, a complex carbohydrate extracted from Aloe vera

引用

INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY 2000年第5期22卷 365-372页

作者： Djeraba, A Quere, P INRA Pathol Aviaire & Parasitol Stn F-37380 Nouzilly France

Acemannan (ACM 1), a beta-(1,4) -acetylated mannan isolated from Aloe vera, can be used as an effective adjuvant in vaccination against some avian viral diseases. Our results demonstrate a quick and lasting in vivo priming effect of ACM 1 on macrophage response after intramuscular inoculation in chickens (500 mu g per 2-month-old bird). In response to IFN-gamma in vitro, monocytes from ACM 1-treated chickens exhibited a strong enhancement of NO production from 3 to 9 days p.i., but a weaker effect on MHC II cell surface antigen expression on day 3 p.i.. A stimulating effect of ACM 1 treatment was also observed on spontaneous and inducible NO production for splenocytes only on day 3 p.i.. By that time, splenocytes exhibited a strong higher capacity to proliferate in response to the T cell-mitogen PHA. At the same time, the in vivo capacity to produce NO, measured by the (NO2-+NO3-) serum level after intravenous LPS injection, increased greatly from 3 to 9 days p.i.. In conclusion, ACM 1 was able efficiently and durably to increase the activation capacity of macrophages from the systemic immune compartment (in particular from the blood and spleen after an intramuscular injection) in chickens, especially for NO production. These findings provide a better understanding of the adjuvant activity of ACM 1 for viral and tumoral diseases. (C) 2000 International Society for Immunopharmacology. Published by Elsevier Science Ltd. All rights reserved.

关键词：佐剂免疫/药理学鸡组织相容性抗原Ⅰ类/分析组织相容性抗原Ⅱ类/分析淋巴细胞活化/药物作用巨噬细胞活化/药物作用甘露聚糖类/药理学单核细胞/代谢一氧化氮/生物合成一氧化氮/血液动物

来源：评论

学校读者我要写书评

暂无评论

Signal transduction induced by immunostimulatory CpG DNA

引用

SPRINGER SEMINARS IN IMMUNOPATHOLOGY 2000年第1-2期22卷 97-105页

作者： Krieg, AM Univ Iowa Coll Med Dept Internal Med Iowa City IA 52242 USA Dept Vet Affairs Med Ctr Iowa City IA 52246 USA CpG Immunopharmaceut Wellesley MA 02481 USA

The immune recognition of unmethylated CpG motifs appears to be an example of the ability of the immune system to detect molecular patterns which are characteristic of microbes, but are not present in vertebrates. This detection is accomplished by the means of pattern recognition receptors (PRR). Unlike some other examples of PRR, immune recognition of CpG DNA appears to require cell uptake and to be accomplished through an intracellular PRR system. This then results in the activation of mitogen-activated protein kinases, culminating in the phosphorylation of transcription factors and the activation of transcription and translation. The rapid activation of these pathways by CpG DNA leads to the induction of protective immune responses.

关键词：佐剂免疫/药理学抗原呈递/药物作用 B淋巴细胞/药物作用 B淋巴细胞/免疫学 CpG岛/免疫学 DNA/免疫学 DNA/药理学树突细胞/药物作用树突细胞/免疫学胞吞作用内颗粒/免疫学基因表达调控/药物作用氢离子浓度淋巴细胞活化/药物作用 MAP激酶信号系统/药物作用巨噬细胞活化/药物作用核酸构象寡脱氧核糖核苷酸类/免疫学寡脱氧核糖核苷酸类/药理学活性氧受体抗原 B细胞/免疫学信号传导/药物作用转录因子/代谢转录遗传/药物作用

来源：评论

学校读者我要写书评

暂无评论

Deficiency of the macrophage migration inhibitory factor gene has no significant effect on endotoxaemia

引用

IMMUNOLOGY 2000年第1期100卷 84-90页

作者： Honma, N Koseki, H Akasaka, T Nakayama, T Taniguchi, M Serizawa, I Akahori, H Osawa, M Mikayama, T Kirin Brewery Co Ltd Pharmaceut Res Lab Gunma Japan Chiba Univ Grad Sch Med Dept Mol Immunol Chiba Japan Chiba Univ Grad Sch Med Dept Mol Embryol Chiba Japan

By targeted disruption of the MIF gene, we have established a mouse strain deficient in macrophage (M phi) migration inhibitory factor (MIF). Despite previous reports indicating an essential role of MIF in endotoxaemia, an injection of lipopolysaccharide (LPS) into the MIF-deficient mice (maintained under specific pathogen-free conditions) caused shock. No significant difference was detected between the MIF-deficient mutant and normal mice in susceptibility to LPS for endotoxaemia or tumour necrosis factor-alpha (TNF-alpha) formation upon LPS injection. Peritoneal M phi from the two strains produced TNF-alpha in response to LPS with similar dose responses. Dexamethasone suppressed the LPS-induced TNF-alpha response of M phi, but no difference was detected between the M phi from the two strains. These results suggest that endogenous MIF has no significant effect on the LPS-induced TNF-alpha production and no effect on suppression of the response by glucocorticoids. Thus, MIF is not crucial for LPS-induced immune responses leading to shock.

关键词：消炎药/药理学地塞米松/药理学内毒素血症/免疫学生育力脂多糖类/免疫学巨噬细胞活化/药物作用巨噬细胞活化/免疫学巨噬细胞游走抑制因子/缺乏巨噬细胞游走抑制因子/遗传学巨噬细胞游走抑制因子/免疫学巨噬细胞腹膜/免疫学小鼠基因敲除休克脓毒性/免疫学存活率肿瘤坏死因子α/生物合成动物小鼠

来源：评论

学校读者我要写书评

暂无评论

Interference in MTT cell viability assay in activated macrophage cell line

引用

ANALYTICAL BIOCHEMISTRY 2003年第2期313卷 338-341页

作者： Pozzolini, M Scarfi, S Benatti, U Giovine, M CNR Direzione Progetto Finalizzato Biotecnol I-16132 Genoa Italy Univ Genoa Dipartimento Med Sperimentale Sezione Biochim I-16132 Genoa Italy

来源：评论

学校读者我要写书评

暂无评论

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

请选择保存的检索档案：

请选择收藏分类：

通借通还

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：