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1.
目的: 观察电离辐射对体外培养的IEC -6细胞株生长的影响及IL- 2对其损伤后增殖和恢复的作用, 并进一步探讨肠黏膜免疫与肠上皮辐射损伤及修复的关系。方法: 用 4、8、12Gy的γ射线照射IEC- 6细胞株, 并于照后 3、6、9、12h及 1、2、3d, 用MTT比色法、光镜、电镜、DNA凝胶电泳和流式细胞术等, 检测受照射后IEC- 6细胞的增殖活力、形态和死亡方式的改变; 用不同浓度IL 2 ( 25×103、5×104、1×105U/L)处理 8Gyγ射线照射的IEC 6细胞, 并于照射后 3、6、9、12、24h, 采用MTT比色法检测其增殖活力的变化。结果: 在 0~12Gy的范围内, IEC 6细胞的增殖活力随γ射线照射剂量的增加而降低。8. 0γ射线照后 24h, 凋亡的IEC- 6细胞明显增多, DNA凝胶电泳显示有梯状带形成。IL- 2可促进照射后的IEC- 6细胞增殖且呈一定的剂量 效应关系, 尤以1×105U/L组的作用更明显。结论: 在一定剂量范围内, γ射线照射可降低IEC 6细胞增殖活力, 且存在剂量 效应关系;可导致IEC 6细胞发生凋亡。IL- 2可促进受照射的IEC- 6细胞增殖, 增强其抗辐射的作用。  相似文献   

2.
IL-2对中子照射后肠上皮细胞生长和凋亡的影响及其机制   总被引:1,自引:0,他引:1  
目的:观察中子照射对体外培养的IEC-6细胞生长的影响及IL-2对其损伤后增殖和恢复的作用,并进一步探讨IL-2调节受照射肠上皮细胞生长的相关机制。方法:单独用IL-2(1×105U/L)或同时施加JAK1激酶阻断剂(A77-1726)处理受4Gy中子照射的IEC-6细胞,并于照后10、15、30min和1、3、6、12、24、48及72h,用MTT比色法和流式细胞术检测受照射后IEC-6细胞的增殖活力和死亡方式的改变。以免疫细胞化学染色和Western blot检测IEC-6细胞上IL-2Rβ的表达和JAK1活化情况。结果:4Gy中子照射后24h,IEC-6细胞的增殖活力明显降低;而IL-2处理组该细胞的增殖活力有显著提高(P<0.05)。受中子照射的IEC-6细胞经IL-2作用24h,其凋亡率明显降低(P<0.05),而坏死率变化不明显。以IL-2刺激中子照射的IEC-6细胞后,于10及15min可见JAK1发生明显磷酸化活化,24h时IL-2Rβ的表达明显增多。同时应用A77-1726和IL-2处理受中子照射的IEC-6细胞后,其增殖活力明显低于单纯IL-2处理组。结论:IL-2可促进受中子照射的IEC-6细胞增殖,具有抗辐射作用。IL-2Rβ和JAK1活化参与了IL-2对中子损伤的IEC-6细胞生长的调控。  相似文献   

3.
To determine the regulatory effects of estrogen and cytokine IL-6 and IL-8 on the growth of epithelial ovarian cancer (OVCA), we first examined the status of estrogen receptors (ERα and ERβ), IL-6 receptor (IL-6Rα and gp130), and IL-8 receptor (IL-8RA and IL-8RB) on five epithelial OVCA cell lines by semiquantitative RT-PCR and Western blot analysis. Results showed that the expressions of these receptors were variable on the five cells. Those OVCA ceUs expressing the receptors were selected to study related molecular mechanism. MTT assay was performed to observe the effects of 17β-estradiol (E2), IL-6 and IL-8 on cell proliferation. We discovered that E2 markedly promoted the proliferation of CAOV-3 and OVCAR-3 cell in a time- and dose-dependent manner. Tamoxifen (Txf), an ER inhibitor, completely blocked the proliferation of the E2-induced cells, and IL-6- or/and IL-8-neutralizing antibody only showed partially blocking activity. IL-6 and IL-8 were able to significantly stimulate CAOV-3 and OVCAR-3 cell proliferation in a time- and dose-dependent manner, which had a potential synergistic effect on CAOV-3 cells but not on OVCAR-3 cells. The cell proliferation induced by these two cytokines was abolished completely by their specific neutralizing antibodies, partially by Txf, but not by unrelated goat IgG. Taken together, our results suggested that estrogen, IL-6 and IL-8 could modulate OVCA growth by forming a reciprocal cascade with amplifying effect.  相似文献   

4.
5.
Several studies have demonstrated that intestinal epithelial cells play a major role in the initiation and perpetuation of intestinal inflammation by secreting proinflammatory cytokines and chemokines. MCP-1 is suggested to be a chemokine that plays a major part during intestinal inflammation in inflammatory bowel disease (IBD). Immunoregulatory cytokines such as IL-4, IL-10 and IL-13 have been described to exert anti-inflammatory properties on various cell types. The aim of our study was to determine the effect of Th2 cytokines on the production of MCP-1 by activated intestinal epithelial cells. We examined Caco-2 cells as well as intestinal epithelial cells which were isolated from surgical specimens. Production of the chemokine MCP-1 was determined under stimulated and non-stimulated conditions. IL-4, IL-10 and IL-13 were added to stimulated epithelial cells under various culture conditions. Supernatants were analysed for cytokine concentrations using ELISAs. Under stimulation with physiological agents like IL-1β or tumour necrosis factor-alpha (TNF-α), we observed markedly increased concentrations of MCP-1 in supernatants of Caco-2 cells and intestinal epithelial cells. IL-4, IL-10 and IL-13 all had the capacity to down-regulate the production of MCP-1 in Caco-2 cells as well as in freshly isolated epithelial cells. Caco-2 cells which were primed with Th2 cytokines 24 h before stimulation were subsequently decreased in their ability to be stimulated by IL-1β or TNF-α for MCP-1 production. As MCP-1 has been shown to play a major role during intestinal inflammation, the in vitro suppression of MCP-1 in enterocytes suggests the in vivo use of regulatory cytokines in patients with active IBD.  相似文献   

6.
In order to assess cytokine-producing cells at the single cell level, the cytokine-specific ELISPOT assay has proven to be an important and sensitive method. The purpose of this study was to adapt this method to elucidate individual cells producing murine IL-2, IL-4 or IL-6. In order to establish these cytokine-specific ELISPOT assays, IL-2-, IL-4- and IL-6-specific cDNA transfected myeloma cell lines, e.g., X63-Ag8-653 X2, X63-Ag8-653 X4 and X63-Ag8-653 X6, respectively, were used as specific cytokine-producing cells. In the IL-2 ELISPOT assay, the coating reagent, monoclonal antibody (mAb) rat IgG2a anti-mouse IL-2 (CR #40014) was used while rabbit IgG polyclonal anti-mouse IL-2 was employed for detection of IL-2 spot forming cells (SFC). The mAbs anti-mouse IL-4, BVD4-1D11 and BVD6-24G2 were selected as capture and detection antibodies for enumeration of IL-4 SFC. For the IL-6 ELISPOT assay, anti-mouse IL-6 (MP5-20F3) mAb was used for coating and MP5-32C11 mAb was used for detection of IL-6 SFC. When IL-2 producing X63-Ag8-653 X2 cells were subjected to these three different ELISPOT assays, IL-2-specific SFC were only noted with the IL-2 ELISPOT system. In the case of IL-4 SFC, only X63-Ag8-653 X4 cells formed specific spots using the tandem of BVD4-1D11 and BVD6-24G2 mAbs. IL-6-specific spots developed in MP5-20F3 mAb pre-coated wells containing X63-Ag8-653 X6 cells, when developed with mAb anti-IL-6 (MP5-32C11). Addition of cycloheximide (50 μg/ml) inhibited formation of IL-2, IL-4 and IL-6 SFC by approximately 90%. When an unrelated mAb was used as detection antibody in these three different cytokine-specific ELISPOT assays, IL-2-, IL-4-and IL-6-specific SFC were not detected. Further, when concanavalin A stimulated T cells from Peyer's patch of normal mice were subjected to the respective cytokine-specific ELISPOT assay, IL-2, IL-4 and IL-6 SFC were enumerated. These results have shown that cytokine-specific IL-2, IL-4 and IL-6 ELISPOT assays have now been established and will allow analysis of the frequency of cytokine-secreting cells at the single cell level.  相似文献   

7.
目的:观察miR-542-5p对1-磷酸鞘氨醇(S1P)诱导的大鼠小肠隐窝上皮IEC-6细胞增殖的影响。方法:建立稳定表达鞘氨醇激酶1(SphK1)的IEC-6细胞系(SphK1-IEC-C1和SphK1-IEC-C2),Western blot检测SphK1蛋白表达,放射性同位素示踪法测定SphK1酶活性和S1P分泌,细胞计数绘制生长曲线观察细胞增殖,流式细胞术分析细胞周期变化,实时荧光定量PCR检测miR-542-5p表达。结果:与对照细胞相比,细胞系SphK1-IECC1和SphK1-IEC-C2中SphK1蛋白表达显著升高,SphK1酶活性升高,细胞内外S1P浓度升高,细胞生长速度加快,细胞周期中S期细胞所占比例升高,miR-542-5p的表达量降低;在IEC-6细胞的培养液中加入S1P(0.5~10μmol/L),能显著抑制miR-542-5p表达;采用siRNA干扰降低IEC-6细胞的SphK1,可明显升高miR-542-5p表达。升高SphK1-IEC-C1和SphK1-IEC-C2细胞中miR-542-5p水平,则可降低S期细胞比例,抑制细胞增殖。结论:S1P通过降低IEC-6细胞中miR-542-5p水平,引起细胞周期由G1期向S期转换,促进IEC-6细胞增殖。  相似文献   

8.
9.
Rapamycin (RAPA) is a potent immunosuppressant. In this study we investigated the effect of RAPA on T cell proliferation triggered by various stimuli in an in vitro human model. The proliferation of T cells stimulated via an alternative pathway using phorbol myristate acetate (PMA) and anti-CD28 antibody (alpha CD28) in the absence of antigen-presenting cells (APC) was strongly inhibited by RAPA. T cell proliferation provoked via a combination of CD3/TCR and CD28 pathways using anti-CD3 antibody (alpha CD3) plus alpha CD28 was also inhibited by RAPA in the presence of APC. The mitogen (phytohaemagglutinin (PHA) or alpha CD3)-induced up-regulation of expression of the IL-2 receptor alpha chain (IL-2R alpha) and the IL-4 receptor (IL-4R) was sensitive to RAPA. This suggests that RAPA's interference with the IL-2 and IL-4 autocrine loops during T cell activation might contribute to RAPA's overall immunosuppressive effect. We have further demonstrated in a two-stage culture system that RAPA strongly inhibited IL-4-stimulated proliferation of T cells, the latter being either pretreated with alpha CD3 in the presence of APC, or with PMA plus alpha CD28 in the absence of APC. The result suggests that the Ca++ influx during the pretreatment is not obligatory for T cells to achieve IL-4 responsiveness. The results also indicate that RAPA's antiproliferative effect on IL-4-stimulated T cells is not contingent on the various mechanisms of cell priming. Therefore, RAPA's major target is probably at the second stage after the priming. Our study has extended current knowledge about the effect of RAPA on human T cells.  相似文献   

10.
A number of cell types situated along interfaces of various tissues and organs such as the peritoneum and the intestine have been shown to secrete inflammatory cytokines in a polarized fashion. Retinal pigment epithelial (RPE) cells are positioned at the interface between the vascularized choroid and the avascular retina, forming part of the blood–retina barrier. These cells are potent producers of inflammatory cytokines and are therefore considered to play an important role in the pathogenesis of ocular inflammation. Whether cytokine secretion by these cells also follows a vectorial pattern is not yet known, and was therefore the subject of this study. Monolayers of human RPE cells (primary cultures and the ARPE-19 cell line) cultured on transwell filters were stimulated to produce IL-6 and IL-8 by adding IL-1β (100 U/ml) to either the upper or the lower compartment. After stimulation, the human RPE cell lines showed polarized secretion of IL-6 and IL-8 towards the basal side, irrespective of the side of stimulation. The ARPE-19 cell line also secreted IL-6 and IL-8 in a polarized fashion towards the basal side after basal stimulation; polarized secretion was, however, not apparent after apical stimulation. The observation that human RPE cells secrete IL-6 and IL-8 in a polarized fashion towards the choroid may represent a mechanism to prevent damage to the adjacent fragile retinal tissue.  相似文献   

11.
王越  杨洁  高燕  牛文彦  姚智 《免疫学杂志》2006,22(5):475-479
目的分析比较五种常见的上皮性卵巢癌细胞系IL-6、IL-8及其受体表达的差异。方法IL-6、IL-8的表达分别采用RT-PCR和ELISA法进行检测,IL-6受体(IL-6Rα和gp130)及IL-8受体(IL-8RA和IL-8RB)的表达采用免疫印迹技术进行测定。结果①五种上皮性卵巢癌细胞均组成性表达IL-6和IL-8。IL-6和IL-8在CAOV-3细胞中的表达水平均最高,而在HO-8910PM细胞中的表达水平均最低,IL-6在SKOV-3、HO-8910、OVCAR-3细胞中的表达水平依次降低,IL-8在OVCAR-3、SKOV-3、HO-8910细胞中的表达水平依次降低。②五种上皮性卵巢癌细胞均表达IL-6Rα、gp130及IL-8RA;除CAOV-3细胞外,其它细胞均表达IL-8RB。结论本研究旨在筛选表达IL-6和IL-8及其相应受体的细胞株,为研究IL-6、IL-8与卵巢癌发生、发展关系奠定基础,同时也为今后卵巢癌的免疫治疗提供一个新的思路。  相似文献   

12.
DHT、IL-6和IL-8对卵巢癌细胞体外增殖的作用   总被引:2,自引:0,他引:2  
目的探讨雄激素与细胞因子在上皮性卵巢癌生长中可能存在的相互调节作用。方法应用免疫印迹(Western blot)和RT-PCR技术对5种常见的上皮性卵巢癌细胞系雄激素受体(AR)、ID6受体(IL-6Rα、gp130)及IL-8受体(IL-8RA、IL-8RB)的表达进行检测,选择兼有AB、IL-6R及IL-8R的卵巢癌细胞系作为研究模型,应用MTT法观察5α-二氢睾酮(5α-dihydrotestosterone,DHT)及IL-6、ID-8两种细胞因子对卵巢癌细胞体外增殖作用的影响。结果(1)5种上皮性卵巢癌细胞系中AR、ID-6Rα、gp130、IL-8RA以及IL-8RB的表达存在差异性。(2)在SKOV-3细胞,低剂量DHT(0.1~1nmol/L)作用后的前72h抑制细胞增殖,中高剂量DHT(1~100nmol/L)作用后的72、96、120h促进细胞增殖;在OVCAR-3细胞,与对照组相比,DHT作用48h时细胞增殖差异无统计学意义,作用96h和144h时才有明显的促增殖作用。DHT对这两种细胞增殖的作用具有明显的剂量依赖性和时间依赖性。(3)AR阻断剂氟他胺(flutamide,Flu)可完全阻断DHT的促增殖作用,而抗IL-6中和抗体和抗IL-8中和抗体则可部分阻断其促增殖作用。(4)ID6和ID8可促进SKOV-3和OVCAR-3细胞增殖,其促增殖作用亦具有一定的剂量依赖性和时间依赖性,且二者在SKOV-3细胞有一定的协同效应,而在OVCAR-3细胞则未见到。ID-6和ID-8诱导的促增殖作用可被其相应的中和抗体完全阻断,而不能被无关抗体即同种型羊IgG所阻断。结论雄激素促进上皮性卵巢癌生长的作用机制可能有二:一是雄激素的直接刺激作用,二是通过调节细胞因子(如ID-6和IL-8)分泌和/或其受体表达量,从而促进细胞的生长。  相似文献   

13.
Ethanol addition to B lymphocytes in vitro inhibits antigen-induced antibody secretion and antigen-induced cell proliferation. We tested the hypothesis that ethanol can inhibit the effect of interleukins on B-cell proliferation by adding ethanol to in vitro functional assays for IL-2 and IL-4. Ethanol does not inhibit IL-2-induced B-cell differentiation, but it does inhibit IL-4-induced B-cell proliferation and IL-4-induced Ig class switching.  相似文献   

14.
目的研究乙型肝炎病毒宫内感染与白细胞介素-4(IL-4)、白细胞介素-6(IL-6)和干扰素-γ(IFN-γ)细胞因子的相关性。方法将研究对象分为两组:研究组为80例乙型肝炎病毒表面抗原(HBsAg)阳性孕妇;对照组为20例正常孕妇。采用双抗夹心酶联免疫吸附法(DAS-ELISA)检测孕妇外周静脉血及其新生儿脐静脉血血清中乙型肝炎五项指标及细胞因子IFN-γ、IL-4、IL-6水平。结果研究组孕妇分娩的新生儿80例有11例宫内感染,宫内感染率为13.75%。新生儿HBV宫内感染组孕妇血清中IFN-γ水平显著低于HBV宫内未感染组及对照组孕妇(P<0.01),IL-4、IL-6水平则显著高于HBV宫内未感染组及对照组孕妇均有统计学意义(P<0.01)。HBV宫内未感染组与对照组相比,上述三种细胞因子水平差异均无统计学意义(P>0.05)。上述各组孕妇血清中IL-4与IL-6水平均呈显著正相关(P<0.01,P<0.01,P<0.01);IFN-γ与IL-4呈显著负相关(P<0.01,P<0.01,P<0.01);IFN-γ与IL-6亦呈显著负相关(P<0.01,P<0.01,P<0.01)。各组新生儿脐血清中IFN-γ、IL-4、IL-6水平差异无统计学意义(P>0.05)。结论孕妇细胞免疫功能紊乱导致IFN-γ抗病毒作用减弱,IL-4、IL-6水平升高,不利于孕妇体内HBV清除,易导致胎儿宫内感染。  相似文献   

15.
Intestinal epithelial cells are known to secrete a variety of cytokines and may play a role in the immune response at the intestinal mucosa. However, the regulatory mechanisms that govern the secretion of these cytokines are largely unknown. In this report, we have focused on the cytokine interactions that regulate interleukin (IL)-6 secretion by the non-transformed rat small intestinal epithelial cell line IEC-6. Tumour necrosis factor-alpha (TNF-alpha) was found to enhance both IL-6 mRNA expression and protein secretion by the IEC-6 cells. Furthermore, TNF-alpha acted in synergy with either transforming growth factor-beta 1 (TGF-beta 1) or IL-1 beta to greatly enhance IEC-6 cell IL-6 secretion. Although the IEC-6 cells are known to produce TGF-beta, autocrine-secreted TGF-beta was found to have no effect on the elevated IL-6 secretion induced by both TNF-alpha plus IL-1 beta. However, the addition of activated TGF-beta 1 to IEC-6 cultures stimulated with both TNF-alpha and IL-1 beta resulted in greatly elevated levels of IL-6 secretion. Therefore, activated TGF-beta 1 can augment IL-6 secretion stimulated by TNF-alpha and IL-1 beta, either alone or in combination, suggesting that intestinal epithelial cell IL-6 secretion may be under the control of a cytokine network at the intestinal mucosa.  相似文献   

16.
IL-1 activity in culture supernatant and cell lysate from rat mesangial cells stimulated with interferon-gamma (IFN-gamma) was measured by a thymocyte proliferation assay. While IFN-gamma alone had no effect on the secretion or the intracellular pool of IL-1, the enhancement by IFN-gamma of IL-1 secretion in response to lipopolysaccharide (LPS) was observed. The stimulatory effect of culture supernatant on thymocyte proliferation was abrogated by preincubation with the anti-IL-1 antibody. At least 4-h incubation with IFN-gamma and LPS was required to detect enhancing effect of IFN-gamma. The addition of as little as 1 U/ml IFN-gamma significantly increased IL-1 secretion in the presence of 10 micrograms/ml LPS. The IL-6 activity in culture supernatants was determined by measurement of thymidine uptake in mouse IL-6-dependent cell line (MH60.BSF2). Mesangial cells secreted IL-6 in culture supernatant without additional stimuli and LPS distinctly increased it as described previously. However, in contrast to IL-1 production, no effect of IFN-gamma on IL-6 secretion was observed in the presence or absence of LPS. Moreover, we determined whether enhanced IL-1 release is associated with Ia expression on mesangial cells. IFN-gamma alone and the combination with LPS induced marked expression of Ia antigen, whereas LPS alone did not. We conclude that IFN-gamma stimulates the production of IL-1, but not IL-6, by mesangial cells and suggest an important role of IFN-gamma in the pathogenesis of glomerulonephritis by regulating the mesangial production of IL-1 and the accessory cell function of mesangial cells.  相似文献   

17.
The murine Helicobacter felis model has been extensively used to investigate the importance of host factors in the development of chronic gastritis. The effect of gender in this murine model is unknown. Male and female C57BL/6J mice were infected with H felis for up to 1 year. At 4, 8, 19, 36, and 52 weeks post-infection, gastric histopathology, epithelial cell proliferation, and apoptosis were examined and compared with age- and gender-matched controls. In female mice, infection with H felis resulted in an earlier onset of chronic gastric inflammation, epithelial hyperplasia, and oxyntic cell loss than males. In females, there was a trend towards increased gastric pathology compared with males, with long-term-infected female mice having significantly greater (p < 0.05) chronic inflammation than male mice. The histopathological differences in male and female mice did not relate to the density of H felis infection. Female mice infected with H felis had significantly increased gastric epithelial cell proliferation in the cardia and corpus at both 8 and 52 weeks post-infection (p < 0.05). Epithelial cell apoptosis in the glandular mucosa of the corpus at 36 and 52 weeks post-infection was significantly increased (p < 0.05) in female mice compared with uninfected gender controls. In contrast, there was no significant increase in epithelial cell proliferation or apoptosis in any area of the stomach at any time point after H felis infection in male mice. These results demonstrate that there are gender differences in the gastric inflammatory and epithelial response to H felis in the murine model. The functional importance of gender should be considered in future murine studies on H felis- and H pylori-induced chronic gastritis.  相似文献   

18.
To study the role of IL-6 in HIV-induced B cell defects, in vitro B cell responses and IL-6 secretion were determined simultaneously in 67 haemophilia patients. Twenty-three patients were HIV- (Group 1), 27 HIV+ stage CDC II, III (Group 2), and 17 were HIV+ stage CDC IV (Group 3). Pokeweed mitogen (PWM) was used for T cell-dependent and Staphylococcus aureus Cowan I (SAC I) for T cell-independent B cell stimulation. B cell differentiation was assessed in a reverse haemolytic plaque assay and by ELISA determination of IgG and IgM in culture supernatants. An ELISA was used to measure IL-6 in plasma and culture supernatants. HIV- patients showed impaired immunoglobulin-secreting cell (ISC) responses after T cell-independent and T cell-dependent stimulation (P < 0.0001 and P < 0.01, respectively), whereas IL-6 secretion, IgM and IgG responses were comparable to those in healthy controls. HIV+ patients at stage CDC II, III or IV demonstrated significantly reduced mitogen-stimulated IL-6 secretion (P < 0.05, PWM; P < or = 0.001, SAC I) as well as impaired ISC and IgG responses (P < 0.01, PWM; P < or = 0.0001, SAC I). CDC IV patients showed reduced IgM responses in addition (P < 0.02, PWM; P < 0.0005, SAC I). Plasma IL-6 levels were elevated both in HIV+ patients (CDC II, III patients: 165 +/- 73 pg/ml, P < 0.005; CDC IV patients: 58 +/- 18 pg/ml, P < 0.0001) and in HIV- patients (283 +/- 65 pg/ml, P < 0.0001) which appeared to be a T cell effect induced by treatment with haemophilia factor concentrates. Our data provide evidence for different types of B cell deficiencies in HIV- patients (impaired ISC response only) and HIV+ patients (impaired ISC as well as IL-6 and IgM/IgG responses). The defective IL-6 secretion in HIV+ patients is likely to affect terminal B cell differentiation and this may explain the reduced immunoglobulin secretion in these patients in response to antigenic challenge.  相似文献   

19.
IL-4 coordinates the Th2-type immune response in inflammatory diseases such as asthma. IL-27 can inhibit the development of both Th2 and Th1 cells. However, IL-27 can also drive naïve T cells to differentiate toward the Th1 phenotype. In this study, we investigated the effects of IL-27 on the activation of IL-4-induced human bronchial epithelial cells (BEAS-2B). Compared to controls, both IL-4 and IL-27 (25–100 ng/mL) increased the concentrations of CCL2 and IL-8 in a dose-dependent manner. However, compared to cells stimulated individually with IL-4 or IL-27, treatment with a combination of both cytokines reduced CCL2 and IL-8 concentrations in a dose- and time-dependent manner. IL-4 increased the activation of p38 MAPK, ERK1/2, STAT6 and NF-κB, while IL-27 increased the activation of p38 MAPK and ERK1/2 but not STAT6 and NF-κB. Compared to IL-4-stimulated cells, cells treated with both IL-27 and IL-4 displayed decreased activation of STAT6 and NF-κB but not ERK1/2 and p38 MAPK. Taken together, these results suggest that IL-27 plays a pro-inflammatory role when administered alone but downregulates bronchial epithelial cell activation when combined with IL-4. Therefore, IL-27 may be an interesting target for the treatment of Th2 inflammatory diseases.  相似文献   

20.
A microfabrication approach was utilized to create topographic analogs of intestinal crypts on a polymer substrate. It was hypothesized that biomimetic crypt-like micro-architecture may induce changes in small intestinal cell (i.e. Caco-2 cell) phenotype. A test pattern of micro-well features with similar dimensions (50, 100, and 500 μm diameter, 50 μm spacing, 120 μm in depth) to the crypt structures found in native basal lamina was produced in the surface of a poly(dimethylsiloxane) (PDMS) substrate. PDMS surfaces were coated with fibronectin, seeded with intestinal-epithelial-cell-like Caco-2 cells, and cultured up to fourteen days. The cells were able to crawl along the steep side walls and migrated from the bottom to the top of the well structures, completely covering the surface by 4–5 days in culture. The topography of the PDMS substrates influenced cell spreading after seeding; cells spread faster and in a more uniform fashion on flat surfaces than on those with micro-well structures, where cell protrusions extending to micro-well side walls was evident. Substrate topography also affected cell metabolic activity and differentiation; cells had higher mitochondrial activity but lower alkaline phosphatase activity at early time points in culture (2–3 days post-seeding) when seeded on micro-well patterned PDMS substrates compared to flat substrates. These results emphasize the importance of topographical design properties of a scaffolds used for tissue engineered intestine.  相似文献   

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