共查询到20条相似文献,搜索用时 15 毫秒
1.
Prof. G. Modat J. Dornand N. Bernad D. Junquero A. Mary A. Muller C. Bonne 《Inflammation research》1990,30(3-4):403-411
Vascular endothelium is known to closely interact with leukocytes and immunocompetent cells. We report here that cultured bovine aortic endothelial cells (BAEC) synthesize both interleukin 1 (IL-1) and interleukin 6 (IL-6) like activities in response to bacterial lipopolysaccharide stimulation. Our results agree with previous data obtained from human venous endothelia and support the concept that IL-1 and IL-6 synthesis are properties common to endothelial cells from different vascular beds. The IL-1 activity was measured by murine thymocyte proliferation assay and by an indirect bioassay using NOB1 cells, which evidenced higher IL-1 amounts than the former. This discrepancy appeared to be partly due to the simultaneous production of one or more inhibitor(s) of the thymocyte proliferation by BAEC. The IL-6 assay was performed with the murine hydridoma cell line B9. In other respects, the cyclooxygenase inhibitor indomethacin enhanced the IL-1 like production, but was ineffective on IL-6 like production. The present study provides additional evidence that endothelial cells from large arteries may also participate in inflammatory and immunological processes. 相似文献
2.
目的:研究脑浆型磷脂酶A2(cytosolic phospholipase A2,cPLA2,85—kD PLA2)在脂多糖诱导Hela细胞释放细胞因子IL-1β、IL-6的信号机制中的作用。方法:①利用脂质体将cPLA2的反义寡核苷酸转染入Hela细胞,通过聚合酶链式反应(RT—PCR)及Western杂交印迹分析检验胞浆中cPLA2人水平的变化;②用放免方法检测不同时间培养上清中的IL-1β、IL-6浓度。结果:①转染后cPLA2的蛋白表达明显减少,但mRNA水平未见显著改变;②Hela细胞释放IL-1β、IL-6随cPLA2人反义寡核苷酸浓度的增加而减少。结论:cPLA2人LPS刺激的Hela细胞释放炎性细胞因子IL-1β、IL-6的过程中可能发挥重要的信号传递作用。 相似文献
3.
Dominguez F Martínez S Quiñonero A Loro F Horcajadas JA Pellicer A Simón C 《Molecular human reproduction》2008,14(7):423-430
The investigation of trophoblast chemoattractive molecules in humans is of high interest for the reproductive field. Current evidence in ruminants demonstrates that CXCL10, formerly the interferon-gamma-inducible protein 10 (IP-10), is a potent chemotactic molecule implicated in the migration of trophoblast cells during early gestation. The aim of this work was to explore the existence of CXCL10/CXCR3 in the human model. Furthermore, chemotaxis assays were performed to demonstrate CXCL10 chemotactic activity in the human trophoblast cell lines JEG-3 and AC-1M88. Surprisingly, the conditioned media from epithelial endometrial cells (EEC) induced the highest trophoblast migration rate. Cytokine and chemokine membrane protein arrays were used to identify the secreted protein profile of EEC-conditioned media, and IL-6 was found to be the most abundant and CXCL13 the second most abundant molecule. Using a chemotaxis assay on AC-IM88, IL-6 antibody blocked the effect of EEC, indicating IL-6 to be an effective chemoattractive factor for trophoblast cells in the human model. 相似文献
4.
TNF刺激肥大细胞IL-6分泌的信号转导通路 总被引:2,自引:0,他引:2
目的:检测TNF对肥大细胞IL-6、IL-10分泌和组胺释放的影响并探讨其可能的信号转导途径。方法:用不同浓度TNF激发肥大细胞系P815后收集细胞和上清,细胞用细胞激发信号ELISA(CASE)方法检测信号转导通路蛋白ERK、p38、和STAT3磷酸化水平,上清用ELISA检测组胺、IL-6和IL-10的水平。结果:ELISA结果显示TNF促进P815肥大细胞IL-6分泌(P<0.05),但对IL-10分泌和组胺释放无明显影响。ERK信号转导通路抑制剂PD98059和U0126抑制TNF引起的P815肥大细胞IL-6分泌(P<0.05),而p38信号转导通路抑制剂SB203580和STAT3信号转导通路抑制剂AG490不能抑制TNF引起的P815肥大细胞IL-6分泌。CASE结果显示ERK信号转导通路抑制剂PD98059,U0126抑制TNF引起的P815肥大细胞内ERK蛋白磷酸化(P<0.05)而p38信号转导通路抑制剂SB203580和STAT3信号转导通路抑制剂AG490不能抑制TNF引起的P815肥大细胞内p38和STAT3蛋白磷酸化。结论:TNF刺激小鼠肥大细胞P815分泌IL-6可能与ERK信号转导通路的激活有关的。 相似文献
5.
Chang JY 《Neuroscience letters》2007,416(3):217-220
Methylmercury (MeHg) is an environmental toxin that causes severe neurological complications in humans and experimental animals. MeHg caused IL-6 release from the rat C6 glioma cells, the human U251HF glioma cells and the human retina pigment epithelial (ARPE-19) cells. These results plus those we reported earlier using mouse N9 microglia cells indicate that IL-6 induction may be a general property of MeHg among various glial cell types across species. MeHg caused a concentration-dependent increase of cellular oxidation with a maximal level reached by approximately 10 microM MeHg, which was similar to that caused by 30 microM H2O2 or t-butyl hydroperoxide (tBH). The ability of MeHg to induce IL-6 release was not affected by exogenously added H2O2 or t-butyl hydroperoxide. Furthermore, IL-6 release was not accompanied by other cytokine release. Given the reports by others that IL-6 could modulate neuronal survival, glia may affect MeHg neurotoxicity by their IL-6 release when exposed to this neurotoxin. 相似文献
6.
Pentoxifylline in vivo down-regulates the release of IL-1 beta, IL-6, IL-8 and tumour necrosis factor-alpha by human peripheral blood mononuclear cells. 总被引:6,自引:0,他引:6 下载免费PDF全文
P Neuner G Klosner E Schauer M Pourmojib W Macheiner C Grünwald R Knobler A Schwarz T A Luger T Schwarz 《Immunology》1994,83(2):262-267
7.
M Coli? N Pejnovi? M Kataranovski N Stojanovi? T Terzi? A Duji? 《International immunology》1991,3(11):1165-1174
To study the in vitro interactions between rat thymic non-lymphoid cells and thymocytes, we established a system for long-term cultivation of thymic epithelial cells (TEC). TEC were cultivated and successfully propagated for over 8 months in RPMI 1640 medium containing 15% FCS, dexamethasone, insulin, epidermal growth factor, and poly-L-lysin as an adhesive matrix. Their epithelial nature has been confirmed using monoclonal anti-cytokeratin (CK) antibodies. More than 95% of these cells were reactive with K 8.13 and CK 8 mAbs, which are pan-epithelial markers for rat TEC in situ. An epithelial cell clone (TE-R 2.5) established from a long-term TEC culture was 100% reactive with these anti-CK antibodies. Phenotypic analysis of TEC cultures was performed by a large panel of mAbs reactive with a subset of rat TEC or CK polypeptides as well as UIex europaeus agglutinin I using a streptavidin-biotin immunofluorescence assay. Although the results obtained demonstrated phenotypic heterogeneity among these cells, most cultures, including the TE-R 2.5 clone, were of subcapsular/medullary phenotype. Medium conditioned by TEC cultures exhibited IL-1 and IL-6 activities when tested on D10S and B9 sensitive cell lines, respectively. Cytokine activities were neutralized (IL-1) or significantly inhibited (IL-6) by specific polyclonal antibodies. In addition, both anti-IL-1 and anti-IL-6 antibodies reacted with TEC in culture and epithelial (CK-positive) cells on thymic cryostat sections, indicating that thymic epithelium provides an important intrathymic source for molecules contributing to T cell activation. 相似文献
9.
Oz-Arslan D Rüscher W Myrtek D Ziemer M Jin Y Damaj BB Sorichter S Idzko M Norgauer J Maghazachi AA 《Journal of leukocyte biology》2006,80(2):287-297
Lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P) are bioactive lipid mediators, which are known to play major roles in allergic reactions as well as in tumor pathogenesis. Here, the biological activities and signal pathways of these lysophospholipids (LPLs) in dendritic cells (DCs) were characterized further. Flow cytometric and immunoblot analyses indicate that immature as well as mature DCs express the LPL receptors S1P1, S1P3, S1P5, and LPA2, but not S1P2, S1P4, LPA1, or LPA3. Moreover, enzyme-linked immunosorbent assay experiments demonstrate that simultaneous addition of these LPLs to immature DCs in the presence of lipopolysaccharide enhanced the secretion of the inflammatory cytokines interleukin (IL)-6 and IL-8 in maturing DCs. In contrast, no modification of IL-6 or IL-8 release was observed after exposure of mature DCs to LPLs alone. In addition, studies with pertussis toxin and mitogen-activated protein kinase (MAPK) kinase inhibitor PD98059 suggested that Gi proteins and MAPK pathway are involved in these LPL-induced cell responses. Corroborating these findings, we observed that LPLs induce the phosphorylation of extracellular signal-regulated kinase 1/2 in immature DCs but not in mature DCs. Further analyses show that inhibitors of phosholipase D, Rho, and protein kinase C also inhibited the LPL-induced release of IL-6 and IL-8. Therefore, our findings suggest that lipopolysaccharide in DCs uncouples LPL receptors from the signal-transducing machinery during maturation and that exposure of LPLs at early time-points to maturing DCs modifies the proinflammatory capacity of mature DCs. 相似文献
10.
The multifunctional cytokine IL-6, which can be locally produced by human bronchial epithelial cells (HBECs), has been found to play a role in IL-4 dependent IgE synthesis. Since the allergic reaction in bronchial asthma is associated with the upregulation of IL-4 and Th2 type of immune response, the purpose of our study was to assess whether IL-4 and related cytokines IL-10 and IL-13 regulate IL-6 release by HBEC s. HBECs were obtained by bronchial brushing, cultured in LHC-9/RPMI 1640. At the third passage the cells were stimulated with cytokines (0.1-20 ng/ml) diluted in unsupplemented media for 24 h. The supernatants were tested for IL-6 content by sandwich ELISA. Unstimulated HBECs produced detectable amounts of IL-6 (368+/-25 pg/ml). Exposure to IL-10 (368+/-22 pg/ml) and IL-13 (395+/-6 pg/ml) resulted in little changes. IL-4 caused a slight but significant increase in IL-6 release (530+/-45 pg/ml), P<0.05, TNFalpha (1657+/-85 pg/ml) and IFNgamma (1953+/-37 pg/ml) showed strong induction of IL-6 release in HBECs (P<0.005 and P<0.001, respectively). Both IL-4 and IL-13 significantly inhibited TNF induced IL-6 release (P<0.01 for both) while augmenting the effect of IFNgamma (P<0.005 and P<0.01, respectively.). IL-10 was without a significant effect. We conclude that Th2-type cytokines IL-4 and IL-13 affect the release of IL-6 by HBECs in response to TNFalpha (inhibition) and IFgamma (augmentation). IL-10 had no effect on the regulation of IL-6 release. Modulation of IL-6 levels by Th2-type cytokines may play a role in allergic reactions through the IL-6 promoting effect on IL-4 mediated IgE production. 相似文献
11.
Mast cells are involved in the development of psoriatic lesion, but it is not known how mast cells are activated or whether mast cell cytokines are expressed during the lesion development. In this study, the Köbner reaction was induced in uninvolved psoriatic skin of 18 patients using the tape‐stripping technique, and a sequence of biopsies was collected at 0 days, 2 h and 3 days or at 0 days, 1 day and 7 days for histochemical analysis. Eight patients developed the Köbner reaction verified at the follow‐up visit 2–2·5 weeks later. No significant differences were observed in total tryptase+ mast cells, psoriasis area and severity index and age/sex. Instead, the percentage of tryptase+ mast cells showing interleukin (IL)‐6 immunoreactivity was significantly higher in biopsies from Köbner‐positive patients than in those from Köbner‐negative patients. IL‐33 is a known inducer of IL‐6 in mast cells, and the number of IL‐33+ cells increased significantly in Köbner‐positive dermal skin at days 3–7. The number of dermal cells with IL‐6 receptor (IL‐6R, CD126) also increased in Köbner‐positive skin at days 3–7. Unexpectedly, the number of IL‐6R+ cells was even higher in Köbner‐negative skin at days 3–7. In the chronic plaque of 10 other psoriatic patients, the numbers of IL‐6+ mast cells and dermal cells showing IL‐6R were higher than those in the non‐lesional skin. In conclusion, the positive Köbner reaction is associated with IL‐6 in mast cells and appearance of IL‐6R+ and IL‐33+ dermal cells. This suggests that a previously unrecognized vicious circle may develop in the early psoriatic lesion. 相似文献
12.
Zhao Y Usatyuk PV Gorshkova IA He D Wang T Moreno-Vinasco L Geyh AS Breysse PN Samet JM Spannhake EW Garcia JG Natarajan V 《American journal of respiratory cell and molecular biology》2009,40(1):19-30
Particulate matter (PM) in ambient air is a risk factor for human respiratory and cardiovascular diseases. The delivery of PM to airway epithelial cells has been linked to release of proinflammatory cytokines; however, the mechanisms of PM-induced inflammatory responses are not well-characterized. This study demonstrates that PM induces cyclooxygenase (COX)-2 expression and IL-6 release through both a reactive oxygen species (ROS)-dependent NF-kappaB pathway and an ROS-independent C/EBPbeta pathway in human bronchial epithelial cells (HBEpCs) in culture. Treatment of HBEpCs with Baltimore PM induced ROS production, COX-2 expression, and IL-6 release. Pretreatment with N-acetylcysteine (NAC) or EUK-134, in a dose-dependent manner, attenuated PM-induced ROS production, COX-2 expression, and IL-6 release. The PM-induced ROS was significantly of mitochondrial origin, as evidenced by increased oxidation of the mitochondrially targeted hydroethidine to hydroxyethidium by reaction with superoxide. Exposure of HBEpCs to PM stimulated phosphorylation of NF-kappaB and C/EBPbeta, while the NF-kappaB inhibitor, Bay11-7082, or C/EBPbeta siRNA attenuated PM-induced COX-2 expression and IL-6 release. Furthermore, NAC or EUK-134 attenuated PM-induced activation of NF-kappaB; however, NAC or EUK-134 had no effect on phosphorylation of C/EBPbeta. In addition, inhibition of COX-2 partly attenuated PM-induced Prostaglandin E2 and IL-6 release. 相似文献
13.
M A Tufano G Cipollaro de l'Ero R Ianniello A Baroni F Galdiero 《Immunopharmacology and immunotoxicology》1992,14(4):769-782
Evaluation was carried out on the action of different antibiotics on the release of cytokines. Experiments were done in vitro on monocytes and on human lymphocytes. Results show that the majority of the antibiotics tested are able to induce the release of one or more cytokines from their respective producing cells. Among the beta-lactams the most active were the cephalosporins (cephalexin, cefamandol, ceftazidin, and a sulbactam-ampicillin combination) in inducing the release of TNF, IL-1 alpha, and IL-6 from monocytes, and releasing IL-4 and IFN-tau from lymphocytes. The sulbactam-ampicillin combination and cefamandole were extremely active in the production of IFN-tau. Among the lincosamides, clindamycine notably stimulated the release of TNF and IL-6, while lincomycine induced a notable increment of IL-4 from monocytes. Teicoplanin is a very strong inducer of TNF, IL-1 alpha and IL-6. 相似文献
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15.
Chang JY 《Neuroscience letters》2011,501(3):152-156
Previous studies have reported that intrahemispheric connections between area 17 (V1, striate cortex) and other cortical visual areas are not point-to-point, but instead have some degree of convergence and divergence. Many pathological conditions can interfere with the normal development of patterns of cortico-cortical connections, but there is little information regarding whether or not early pathological insults can also induce permanent changes in the convergence and divergence of cortical connections. Obtaining this information is important because loss of precision in neural projections can contribute to functional deficits and behavioral impairment. In the present study we investigated whether retinal input is required for the development of normal values of convergence and divergence in the visual callosal pathway. We found that enucleation performed at birth induced significant increases in convergence and divergence compared to control animals. In contrast, values of convergence and divergence in rats enucleated at postnatal day 7 (P7) were similar to those in controls. Previous studies have shown that retinal input during the first postnatal week is required for the specification of the overall distribution and internal topography of visual callosal pathways. Our present results therefore extend these previous finding by showing that retinal input during the first postnatal week also specifies the precision of cortico-cortical projections. These findings raise the possibility that the precision of neural connections may be reduced in other pathological conditions that affect early development of neural connections. 相似文献
16.
Methylmercury (MeHg) is a neurotoxin capable of causing severe damage to the CNS, especially in the developing fetus. Glia in the CNS release a number of cytokines that are important for proper CNS development and function. We reported earlier that MeHg could induce interleukin-6 (IL-6) release in primary mouse glia. This finding is significant considering previous reports indicating that sustained IL-6 exposure could be detrimental to cerebellar granule neurons, one of the major cellular targets of MeHg cytotoxicity. By using pharmacological antagonists against phophatidycholine- and phosphoinositol-specific phospholipase C, the current study indicated that phospholipase C activity was necessary for MeHg-induced IL-6 release. Results from pharmacological antagonists further suggested that the calcium signaling initiated by phospholipase C appeared essential for this event. In contrast, protein kinase C activity did not appear to be important. Even though mitogen-activated protein kinases were important for IL-6 release in some experimental systems, these enzymes did not appear to be required for MeHg-induced IL-6 release in glia. Based on these data and those reported by us and others, there is a possibility that MeHg-induced phospholipase C activation initiates a calcium signaling that causes phospholipase A2 activation. This, in turn, leads to arachidonic acid and lysophosphatidyl choline generation, both of which are potent inducers for IL-6 release. 相似文献
17.
Tanaka S Mikura S Hashimoto E Sugimoto Y Ichikawa A 《European journal of immunology》2005,35(2):460-468
We previously demonstrated that histamine synthesis is drastically induced upon sensitization with an anti-DNP IgE clone, SPE-7, in IL-3-dependent mouse bone marrow derived mast cells (BMMC). We found that Ca2+ mobilization induced by SPE-7 exhibited a similar profile to the capacitative Ca2+ entry evoked by thapsigargin. Potentials for activation of mast cells were found to vary between different IgE clones, and a monovalent hapten, DNP-lysine, suppressed the activation induced by SPE-7. Ca2+ mobilization induced by SPE-7 was suppressed potently by the specific store-operated Ca2+ channel inhibitor, SK&F 96365, but not at all by Ca2+ channel inhibitors with more broad spectrum, La3+ and Gd3+, whereas the Ca2+ mobilization induced by Ag stimulation was suppressed by these inhibitors. Ca2+ mobilization was also induced by SPE-7 in in vitro differentiated mast cells, although the increases in histamine synthesis and IL-6 release were smaller than those in BMMC. These results suggest that Ca2+ influx operated by a distinct mechanism from that in Ag stimulation is essential for increased histamine synthesis and IL-6 release in mast cells. 相似文献
18.
白细胞介素-6诱导相关新基因LX3的细胞定位研究 总被引:1,自引:0,他引:1
目的 研究IL-6诱导相关新基因KX3在真核细胞内的表达定位。方法构建真核融合表达载体pEGFP-N1/LX3,运用Lipofectin转染293T和NIH3T3细胞。共聚焦荧光显微镜检测GFP荧光,以确定IL-6诱导相关新基因KX3在细胞内的表达定位情况。结果获得真核表达载体pEGFP-N1/LX3,并成功转染293T和NIH3T3细胞,共聚焦荧光显微镜观察了KX3-GFP在细胞内的荧光分布。结论IL-6诱导相关新基因在细胞内为全细胞分布。 相似文献
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20.
T G Yin 《Immunological investigations》1990,19(5-6):413-419
IL-6 production by antigen-specific and antigen-non-specific B cells was studied. It was found that low concentrations of antigen (0.001 micrograms/ml) could stimulate IL-6 production by antigen-specific B cells (10(3)-10(4) fold lower concentration of antigen when compared with that of antigen-nonspecific B cells). A kinetic study showed that IL-6 activity in supernatants from antigen-specific B cells was detectable as early as 2 hours. The production of IL-6 by non-specific B cells and by monocytes was distinctly different. These results suggest that antigen-specific B cells may play a critical role in early T cell activation by antigen. 相似文献