International Journal of Inflammation最新文献_第10页

Association of Alanine Aminotransferase and Periodontitis: A Cross-Sectional Analysis—NHANES 2009–2012 丙氨酸转氨酶与牙周炎的相关性:横断面分析- nhanes 2009-2012

IF 2 Q3 IMMUNOLOGY

International Journal of Inflammation

Pub Date : 2016-02-11 DOI: 10.1155/2016/3901402

R. Wiener, U. Sambamoorthi, R. Jurevic, Robert C Byrd

Objective. Alanine Aminotransferase is an enzyme associated with not only liver diseases, liver conditions, and metabolic syndrome, but also inflammation. Periodontitis is associated with increased cytokines and other markers of inflammation. The purpose of this study is to determine if an independent association between Alanine Aminotransferase and periodontitis exists. Methods. Data from the 2009-2010 and 2011-2012 National Health and Nutrition Surveys (NHANES) were combined. Data concerning periodontitis and Alanine Aminotransferase were extracted and analyzed with Rao Scott Chi-square and logistic regressions. Serum Alanine Aminotransferase was dichotomized at 40 units/liter, and periodontitis was dichotomized to the presence or absence of periodontitis. Results. In bivariate Chi-square analyses, periodontitis and Alanine Aminotransferase were associated (p = 0.0360) and remained significant in unadjusted logistic regression (OR = 1.30 [95% CI: 1.02, 1.65]). However, when other known risk factors of periodontitis were included in the analyses, the relationship attenuated and failed to reach significance (adjusted OR = 1.17 [95% CI: 0.85, 1.60]). Conclusion. Our study adds to the literature a positive but attenuated association of serum Alanine Aminotransferase with periodontitis which failed to reach significance when other known, strong risk factors of periodontitis were included in the analysis.

目标。丙氨酸转氨酶是一种酶，不仅与肝脏疾病、肝脏状况和代谢综合征有关，而且与炎症有关。牙周炎与细胞因子和其他炎症标志物的增加有关。本研究的目的是确定丙氨酸转氨酶与牙周炎之间是否存在独立的关联。方法。2009-2010年和2011-2012年国家健康和营养调查(NHANES)的数据被合并。提取有关牙周炎和丙氨酸转氨酶的数据，并采用Rao Scott卡方和logistic回归进行分析。血清丙氨酸转氨酶在40单位/升时进行二分类，并根据有无牙周炎进行牙周炎二分类。结果。在双变量卡方分析中，牙周炎和丙氨酸转氨酶相关(p = 0.0360)，在未调整的logistic回归中仍然显著(OR = 1.30 [95% CI: 1.02, 1.65])。然而，当其他已知的牙周炎危险因素被纳入分析时，相关性减弱，未能达到显著性(校正OR = 1.17 [95% CI: 0.85, 1.60])。结论。我们的研究为文献增加了血清丙氨酸转氨酶与牙周炎的正相关性，但相关性减弱，当其他已知的牙周炎的强危险因素被纳入分析时，这一相关性未能达到显著性。

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引用次数: 6

The Pattern of Juvenile Idiopathic Arthritis in a Single Tertiary Center in Saudi Arabia 沙特阿拉伯单一三级中心的青少年特发性关节炎的模式

IF 2 Q3 IMMUNOLOGY

International Journal of Inflammation

Pub Date : 2016-02-07 DOI: 10.1155/2016/7802957

Mohammad H. Al-Hemairi, S. Albokhari, M. Muzaffer

Introduction. Juvenile Idiopathic Arthritis (JIA) is the most common chronic arthritis in children. Our aim is to describe demographic, clinical, and laboratory characteristics and treatment of JIA patients followed up in Pediatric Rheumatology clinic in a tertiary center in Saudi Arabia. Methods. Medical records of all patients who are followed up between January 2007 and January 2015 were retrospectively reviewed. Data were collected about demographic, clinical, and laboratory features and treatment. Results. Total patients were 82, males were 31 (37.8%), and mean age of JIA onset was 7.1 ± 3.6 yr. Mean follow-up duration was 2.67±1.6 yr. Systemic onset JIA (SoJIA) was the commonest (36.5%), followed by polyarticular in 29.2% and oligoarticular in 28%. Large and small joints are involved in 76 (92%) and 30 (36.6%), respectively. Main extra-articular feature was fever in 34 (41.4%). Uveitis was diagnosed in 7 (8.5%) and in 5 (21.7%) of oligoarticular JIA. Anemia was found in 49 (59.7%), high ESR in 45 (54.8%), and leukocytosis and thrombocytosis in 33 (40.2%). Positive ANA was found in 30 (36.5%) mainly in oligoarticular subtype as 12 (52%) patients (out of 23) had this positive test. 9 patients (10.9%) required NSAIDs only, 6 patients (7.3%) required NSAIDs and intra-articular steroids only, and 19 (23%) required NSAIDs, methotrexate, steroids, and biologics. Conclusion. SoJIA is the most common JIA subtype in our study. A population based rather than a single center study will give more details about JIA characteristics in Saudi Arabia

介绍。幼年特发性关节炎(JIA)是儿童中最常见的慢性关节炎。我们的目的是描述在沙特阿拉伯三级中心儿童风湿病诊所随访的JIA患者的人口学、临床和实验室特征和治疗。方法。回顾性分析2007年1月至2015年1月期间随访的所有患者的医疗记录。收集有关人口统计学、临床、实验室特征和治疗的数据。结果。总病例82例，男性31例(37.8%)，JIA平均发病年龄为7.1±3.6年，平均随访时间为2.67±1.6年。全身性JIA (SoJIA)最常见(36.5%)，其次是多关节性(29.2%)和少关节性(28%)。大关节76例(92%)，小关节30例(36.6%)。34例(41.4%)以发热为主要关节外特征。7例(8.5%)和5例(21.7%)被诊断为葡萄膜炎。贫血49例(59.7%)，高ESR 45例(54.8%)，白细胞增多和血小板增多33例(40.2%)。ANA阳性30例(36.5%)，主要发生在寡关节亚型，其中12例(52%)患者(23例)检测呈阳性。9例(10.9%)患者仅需要使用非甾体抗炎药，6例(7.3%)患者仅需要使用非甾体抗炎药和关节内类固醇，19例(23%)患者需要使用非甾体抗炎药、甲氨蝶呤、类固醇和生物制剂。结论。SoJIA是我们研究中最常见的JIA亚型。基于人群而非单中心的研究将提供沙特阿拉伯JIA特征的更多细节

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引用次数: 28

Investigation of the Anti-Inflammatory and Analgesic Activities of Ethanol Extract of Stem Bark of Sonapatha Oroxylum indicum In Vivo 白刺干皮乙醇提取物体内抗炎镇痛活性的研究

IF 2 Q3 IMMUNOLOGY

International Journal of Inflammation

Pub Date : 2016-01-26 DOI: 10.1155/2016/8247014

K. Lalrinzuali, M. Vabeiryureilai, G. Jagetia

Inflammation is all a pervasive phenomenon, which is elicited by the body in response to obnoxious stimuli as a protective measure. However, sustained inflammation leads to several diseases including cancer. Therefore it is necessary to neutralize inflammation. Sonapatha (Oroxylum indicum), a medicinal plant, is traditionally used as a medicine in Ayurveda and other folk systems of medicine. It is commonly used to treat inflammatory diseases including rheumatoid arthritis and asthma. Despite this fact its anti-inflammatory and analgesic effects are not evaluated scientifically. Therefore, the anti-inflammatory and analgesic activities of Sonapatha (Oroxylum indicum) were studied in Swiss albino mice by different methods. The hot plate, acetic acid, and tail immersion tests were used to evaluate the analgesic activity whereas xylene-induced ear edema and formalin induced paw edema tests were used to study the anti-inflammatory activity of Sonapatha. The administration of mice with 250 and 300 mg/kg b.wt. of O. indicum reduced pain and inflammation indicating that Sonapatha possesses analgesic and anti-inflammatory activities. The maximum analgesic and anti-inflammatory activities were observed in mice receiving 300 mg/kg b.wt. of O. indicum ethanol extract. Our study indicates that O. indicum possesses both anti-inflammatory and analgesic activities and it may be useful as an anti-inflammatory agent in the inflammation related disorders.

炎症是一种普遍存在的现象，它是身体对令人讨厌的刺激作出反应而引起的，是一种保护措施。然而，持续的炎症会导致包括癌症在内的几种疾病。因此，有必要中和炎症。Sonapatha (Oroxylum indicum)是一种药用植物，传统上在阿育吠陀和其他民间医学系统中被用作药物。它通常用于治疗炎性疾病，包括类风湿关节炎和哮喘。尽管如此，它的抗炎和镇痛作用还没有得到科学的评价。为此，采用不同方法对瑞士白化小鼠的抗炎、镇痛作用进行了研究。采用热板法、醋酸法和尾浸没法评价其镇痛活性，采用二甲苯致耳水肿法和福尔马林致足水肿法研究其抗炎活性。250和300 mg/kg b.wt给药小鼠。表明索纳帕塔具有镇痛和抗炎活性。给药300 mg/kg b.wt的小鼠观察到最大的镇痛和抗炎作用。梧桐乙醇提取物。本研究表明，该植物具有抗炎和镇痛双重作用，可能是治疗炎症相关疾病的有效药物。

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引用次数: 44

Intravenous Immunoglobulins: Mode of Action and Indications in Autoimmune and Inflammatory Dermatoses 静脉注射免疫球蛋白:自身免疫性和炎症性皮肤病的作用模式和适应症

IF 2 Q3 IMMUNOLOGY

International Journal of Inflammation

Pub Date : 2016-01-18 DOI: 10.1155/2016/3523057

L. Dourmishev, D. Guleva, L. Miteva

Intravenous immunoglobulins (IVIGs), a mixture of variable amounts of proteins (albumin, IgG, IgM, IgA, and IgE antibodies), as well as salt, sugar, solvents, and detergents, are successfully used to treat a variety of dermatological disorders. For decades, IVIGs have been administered for treatment of infectious diseases and immune deficiencies, since they contain natural antibodies that represent a first-line defense against pathogens. Today their indication has expanded, including the off-label therapy for a variety of autoimmune and inflammatory diseases. In dermatology, IVIGs are administered for treatment of different disorders at different therapeutic regimens, mostly with higher doses then those administered for treatment of infectious diseases. The aim of this prospective review is to highlight the indications, effectiveness, side effects, and perspectives of the systemic treatment with IVIGs for patients with severe, life-threatening, and resistant to conventional therapies autoimmune or inflammatory dermatoses.

静脉注射免疫球蛋白(IVIGs)是一种由不同数量的蛋白质(白蛋白、IgG、IgM、IgA和IgE抗体)以及盐、糖、溶剂和洗涤剂组成的混合物，已成功地用于治疗各种皮肤病。几十年来，免疫球蛋白一直被用于治疗传染病和免疫缺陷，因为它们含有天然抗体，是对抗病原体的第一道防线。今天，它们的适应症已经扩大，包括各种自身免疫性疾病和炎症性疾病的适应症外治疗。在皮肤病学中，ivg以不同的治疗方案用于治疗不同的疾病，其剂量大多高于用于治疗传染病的剂量。这篇前瞻性综述的目的是强调IVIGs对严重的、危及生命的、对常规疗法有抵抗力的自身免疫性或炎症性皮肤病患者的适应证、有效性、副作用和全身治疗的前景。

引用次数: 27

Nicotine Inhibits Clostridium difficile Toxin A-Induced Colitis but Not Ileitis in Rats 尼古丁抑制艰难梭菌毒素a诱导的大鼠结肠炎但不抑制回肠炎

IF 2 Q3 IMMUNOLOGY

International Journal of Inflammation

Pub Date : 2016-01-11 DOI: 10.1155/2016/4705065

Steven R Vigna

Nicotine is protective in ulcerative colitis but not Crohn's disease of the small intestine, but little is known about the effects of nicotine on Clostridium difficile toxin A-induced enteritis. Isolated ileal or colonic segments in anesthetized rats were pretreated with nicotine bitartrate or other pharmacological agents before intraluminal injection of toxin A. After 3 hours, the treated segments were removed and inflammation was assessed. Nicotine biphasically inhibited toxin A colitis but not ileitis. Pretreatment with the nicotinic receptor antagonist, hexamethonium, blocked the effects of nicotine. Pretreating the colonic segments with hexamethonium before toxin A administration resulted in more inflammation than seen with toxin A alone, suggesting that a tonic nicotinic anti-inflammatory condition exists in the colon. Nicotine also inhibited toxin A-induced increased colonic concentrations of the TRPV1 (transient receptor potential vanilloid subtype 1) agonist, leukotriene B4 (LTB4), and release of the proinflammatory neuropeptide, substance P. Pretreatment with nicotine did not protect against direct TRPV1-mediated colitis caused by intraluminal capsaicin. Nicotinic cholinergic receptors tonically protect the colon against inflammation and nicotine inhibits toxin A colitis but not toxin A ileitis in rats in part by inhibition of toxin A-induced activation of TRPV1 by endogenous TRPV1 agonists such as LTB4.

尼古丁对溃疡性结肠炎有保护作用，但对小肠克罗恩病没有保护作用，但对尼古丁对艰难梭菌毒素a引起的肠炎的影响知之甚少。麻醉大鼠离体回肠或结肠段先用重酒石酸尼古丁或其他药物预处理，然后腔内注射毒素a。3小时后取出处理段，评估炎症反应。尼古丁双相抑制毒素A型结肠炎，但不抑制回肠炎。用尼古丁受体拮抗剂六甲溴铵预处理可阻断尼古丁的作用。在毒素A给药前用六甲铵预处理结肠段导致比单独使用毒素A更严重的炎症，表明结肠中存在补益性烟碱抗炎状态。尼古丁还能抑制毒素a诱导的TRPV1(瞬时受体电位香草酸亚型1)激动剂白三烯B4 (LTB4)的结肠浓度升高，以及促炎神经肽p物质的释放。尼古丁预处理不能预防由腔内辣椒素引起的TRPV1介导的直接结肠炎。尼古丁胆碱能受体能强直地保护结肠免受炎症，尼古丁抑制毒素A结肠炎，但不抑制毒素A回肠炎，部分原因是内源性TRPV1激动剂(如LTB4)抑制毒素A诱导的TRPV1激活。

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引用次数: 4

Inflammatory Serum Protein Profiling of Patients with Lumbar Radicular Pain One Year after Disc Herniation. 腰椎间盘突出后1年腰神经根痛患者的炎性血清蛋白谱分析。

IF 2 Q3 IMMUNOLOGY

International Journal of Inflammation

Pub Date : 2016-01-01 Epub Date: 2016-05-11 DOI: 10.1155/2016/3874964

Aurora Moen, Anne-Li Lind, Måns Thulin, Masood Kamali-Moghaddam, Cecilie Røe, Johannes Gjerstad, Torsten Gordh

Earlier studies suggest that lumbar radicular pain following disc herniation may be associated with a local or systemic inflammatory process. In the present study, we investigated the serum inflammatory protein profile of such patients. All 45 patients were recruited from Oslo University Hospital, Ullevål, Norway, during the period 2007-2009. The new multiplex proximity extension assay (PEA) technology was used to analyze the levels of 92 proteins. Interestingly, the present data showed that patients with radicular pain 12 months after disc herniation may be different from other patients with regard to many measurable serum cytokines. Given a false discovery rate (FDR) of 0.10 and 0.05, we identified 41 and 13 proteins, respectively, which were significantly upregulated in the patients with severe pain one year after disc herniation. On the top of the list ranked by estimated increase we found C-X-C motif chemokine 5 (CXCM5; 217% increase), epidermal growth factor (EGF; 142% increase), and monocyte chemotactic protein 4 (MCP-4; 70% increase). Moreover, a clear overall difference in the serum cytokine profile between the chronic and the recovered patients was demonstrated. Thus, the present results may be important for future protein serum profiling of lumbar radicular pain patients with regard to prognosis and choice of treatment. We conclude that serum proteins may be measurable molecular markers of persistent pain after disc herniation.

早期的研究表明，腰椎间盘突出后的腰根性疼痛可能与局部或全身炎症过程有关。在本研究中，我们研究了这些患者的血清炎症蛋白谱。所有45名患者均于2007-2009年期间从挪威ullev的奥斯陆大学医院招募。采用新的多重接近扩展试验(PEA)技术分析了92种蛋白的水平。有趣的是，目前的数据显示，椎间盘突出后12个月的神经根性疼痛患者在许多可测量的血清细胞因子方面可能与其他患者不同。在假发现率(FDR)为0.10和0.05的情况下，我们分别鉴定出41个和13个蛋白，它们在椎间盘突出一年后出现严重疼痛的患者中显著上调。在估计增加的列表中，我们发现C-X-C基序趋化因子5 (CXCM5;增加217%)，表皮生长因子(EGF;增加142%)，单核细胞趋化蛋白4 (MCP-4;增加70%)。此外，慢性和康复患者之间的血清细胞因子谱有明显的总体差异。因此，目前的结果可能对腰椎神经根性疼痛患者的预后和治疗选择具有重要意义。我们得出结论，血清蛋白可能是椎间盘突出后持续疼痛的可测量的分子标志物。

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引用次数: 46

EOLA1 Inhibits Lipopolysaccharide-Induced Vascular Cell Adhesion Molecule-1 Expression by Association with MT2A in ECV304 Cells EOLA1通过与MT2A联合抑制ECV304细胞中脂多糖诱导的血管细胞粘附分子-1的表达

IF 2 Q3 IMMUNOLOGY

International Journal of Inflammation

Pub Date : 2015-12-31 DOI: 10.1155/2015/301562

Weiling Leng, Xiaotian Lei, Hao Meng, Xinshou Ouyang, Z. Liang

Our research group firstly discovered endothelial-overexpressed lipopolysaccharide-associated factor 1 (EOLA1, GenBank number AY074889) as a lipopolysaccharide (LPS) responsive gene in ECV304 cells. The previous studies have further demonstrated the association of EOLA1 with metallothionein 2A (MT2A), while the role of EOLA1 during LPS-induced inflammatory response in ECV304 cells is unknown. In this report, we determined the subcellular localization of EOLA1 and the regulatory capacity of EOLA1 on vascular cell adhesion molecule-1 (VCAM-1) in response to LPS in ECV304 cells. Our results show that EOLA1 is broadly diffuse in the cells, and EOLA1 expression is dramatically induced by LPS. EOLA1 knockdown results in significant enhancement of LPS-induced VCAM-1 production. Consistent with this, overexpression of EOLA1 leads to the reduction of LPS-induced VCAM-1 production. Furthermore, MT2A knockdown reduces LPS-induced VCAM-1 production. Collectively, our results demonstrate a negative regulatory role of EOLA1 on LPS-induced VCAM-1 expression involving its association with MT2A in ECV304 cells.

本课题组首次在ECV304细胞中发现内皮过表达的脂多糖相关因子1 (EOLA1, GenBank编号AY074889)作为脂多糖(LPS)应答基因。先前的研究进一步证实了EOLA1与金属硫蛋白2A (metallothionein 2A, MT2A)的关联，而EOLA1在lps诱导的ECV304细胞炎症反应中的作用尚不清楚。在本报告中，我们在ECV304细胞中测定了EOLA1的亚细胞定位以及EOLA1对血管细胞粘附分子-1 (VCAM-1)响应LPS的调节能力。我们的研究结果表明，EOLA1在细胞中广泛弥散，并且LPS显著诱导EOLA1的表达。EOLA1敲低导致lps诱导的VCAM-1产生显著增强。与此一致的是，过表达EOLA1导致lps诱导的VCAM-1产生减少。此外，MT2A敲除可减少lps诱导的VCAM-1产生。总之，我们的研究结果表明EOLA1对lps诱导的ECV304细胞中VCAM-1表达的负调控作用涉及其与MT2A的关联。

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引用次数: 6

Angiogenesis in Inflammatory Bowel Disease 炎症性肠病中的血管生成

IF 2 Q3 IMMUNOLOGY

International Journal of Inflammation

Pub Date : 2015-12-29 DOI: 10.1155/2015/970890

C. Alkim, H. Alkim, A. Koksal, S. Boga, I. Sen

Angiogenesis is an important component of pathogenesis of inflammatory bowel disease (IBD). Chronic inflammation and angiogenesis are two closely related processes. Chronic intestinal inflammation is dependent on angiogenesis and this angiogenesis is modulated by immune system in IBD. Angiogenesis is a very complex process which includes multiple cell types, growth factors, cytokines, adhesion molecules, and signal transduction. Lymphangiogenesis is a new research area in the pathogenesis of IBD. While angiogenesis supports inflammation via leukocyte migration, carrying oxygen and nutrients, on the other hand, it has a major role in wound healing. Angiogenic molecules look like perfect targets for the treatment of IBD, but they have risk for serious side effects because of their nature.

血管生成是炎症性肠病(IBD)发病机制的重要组成部分。慢性炎症和血管生成是两个密切相关的过程。慢性肠道炎症依赖于血管生成，而这种血管生成是由免疫系统调节的。血管生成是一个非常复杂的过程，涉及多种细胞类型、生长因子、细胞因子、粘附分子和信号转导。淋巴管生成是IBD发病机制研究的一个新领域。虽然血管生成通过白细胞迁移，携带氧气和营养物质来支持炎症，但另一方面，它在伤口愈合中起主要作用。血管生成分子看起来是治疗IBD的完美目标，但由于它们的性质，它们有严重副作用的风险。

引用次数: 104

VEGFR-2 Expression in Glioblastoma Multiforme Depends on Inflammatory Tumor Microenvironment 多形性胶质母细胞瘤中VEGFR-2的表达与炎性肿瘤微环境有关

IF 2 Q3 IMMUNOLOGY

International Journal of Inflammation

Pub Date : 2015-12-22 DOI: 10.1155/2015/385030

J. Jaal, M. Kase, A. Minajeva, M. Saretok, A. Adamson, Jelizaveta Junninen, T. Metsaots, T. Jõgi, M. Joonsalu, M. Vardja, T. Asser

Glioblastoma multiforme (GBM) is one of the most angiogenic tumors. However, antiangiogenic therapy has not shown significant clinical efficacy. The aim of our study was to evaluate the impact of inflammatory tumor microenvironment on the expression of vascular endothelial growth factor receptor 2 (VEGFR-2). Surgically excised primary GBM tissues were histologically examined for overall extent of inflammation (score 1–3). After immunohistochemistry, the tissue expression of ICAM-1 (optical density), the number of VEGFR-2 positive (VEGFR-2+) blood vessels (per microscopic field), and the endothelial staining intensity of VEGFR-2 (score 0–3) were determined. In GBM, the extent of inflammation was 1.9 ± 0.7 (group mean ± SD). Mean optical density of inflammatory mediator ICAM-1 was 57.0 ± 27.1 (pixel values). The number of VEGFR-2+ blood vessels and endothelial VEGFR-2 staining intensity were 6.2 ± 2.4 and 1.2 ± 0.8, respectively. A positive association was found between endothelial VEGFR-2 staining intensity and the extent of inflammation (p = 0.005). Moreover, VEGFR-2 staining intensity correlated with the expression level of ICAM-1 (p = 0.026). The expression of VEGFR-2, one of the main targets of antiangiogenic therapy, depends on GBM microenvironment. Higher endothelial VEGFR-2 levels were seen in the presence of more pronounced inflammation. Target dependence on inflammatory tumor microenvironment has to be taken into consideration when treatment approaches that block VEGFR-2 signaling are designed.

多形性胶质母细胞瘤(GBM)是最具血管生成性的肿瘤之一。然而，抗血管生成治疗尚未显示出显著的临床疗效。我们的研究目的是评估炎症性肿瘤微环境对血管内皮生长因子受体2 (VEGFR-2)表达的影响。手术切除的原发性GBM组织进行组织学检查，检查炎症的总体程度(评分1-3)。免疫组化后，测定ICAM-1的组织表达(光密度)、VEGFR-2阳性(VEGFR-2+)血管数(每镜场)和VEGFR-2内皮染色强度(评分0-3)。GBM组炎症程度为1.9±0.7(组平均±SD)。炎症介质ICAM-1的平均光密度为57.0±27.1(像素值)。VEGFR-2阳性血管数为6.2±2.4，内皮细胞VEGFR-2染色强度为1.2±0.8。内皮细胞VEGFR-2染色强度与炎症程度呈正相关(p = 0.005)。VEGFR-2染色强度与ICAM-1表达水平相关(p = 0.026)。VEGFR-2的表达依赖于GBM微环境，是抗血管生成治疗的主要靶点之一。较高的内皮细胞VEGFR-2水平出现在更明显的炎症。在设计阻断VEGFR-2信号的治疗方法时，必须考虑对炎性肿瘤微环境的靶标依赖性。

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引用次数: 8

CCR7 Receptor Expression in Mono-MAC-1 Cells: Modulation by Liver X Receptor α Activation and Prostaglandin E2 CCR7受体在单核mac -1细胞中的表达:肝X受体α活化和前列腺素E2的调节

IF 2 Q3 IMMUNOLOGY

International Journal of Inflammation

Pub Date : 2015-12-06 DOI: 10.1155/2015/201571

Bérengère Tanné, S. Bernier, Nancy Dumais

Cell migration via chemokine receptor CCR7 expression is an essential function of the immune system. We previously showed that prostaglandin E2 (PGE2), an important immunomodulatory molecule, increases CCR7 expression and function in monocytes. Here, we explore the role of the liver X receptor α (LXRα) activation on CCR7 expression in Mono-Mac-1 (MM-1) cells in the presence of PGE2. To do this, MM-1 cells were stimulated with the LXRα synthetic agonist T0901317 in the presence or absence of PGE2. CCR7 mRNA transcription was measured using quantitative RT-PCR and protein expression was examined using flow cytometry. CCR7 function was analyzed using migration assays in response to CCL19/CCL21, which are natural ligands for CCR7. Our results show that agonist-mediated activation of LXRα in the presence of PGE2 increases CCR7 mRNA transcription and MM-1 cell migratory capacity in response to CCL19/21. In addition, our results demonstrate that engagement of the E-prostanoids 2 and 4 (EP2/EP4) receptors present on MM-1 cells is responsible for the observed increase in CCR7 mRNA expression and function during LXRα activation. Examination of monocyte migration in response to lipid derivatives such as PGE2 and oxysterols that are produced at sites of chronic inflammation would contribute to understanding the excessive monocyte migration that characterizes atherosclerosis.

通过趋化因子受体CCR7表达的细胞迁移是免疫系统的重要功能。我们之前的研究表明，前列腺素E2 (PGE2)是一种重要的免疫调节分子，可以增加单核细胞中CCR7的表达和功能。本研究探讨PGE2存在下肝脏X受体α (LXRα)激活对单核细胞-1 (MM-1) CCR7表达的影响。为此，在PGE2存在或不存在的情况下，用LXRα合成激动剂T0901317刺激MM-1细胞。定量RT-PCR检测CCR7 mRNA转录，流式细胞术检测CCR7蛋白表达。CCR7的天然配体CCL19/CCL21通过迁移实验分析了CCR7的功能。我们的研究结果表明，在PGE2存在的情况下，激动剂介导的LXRα激活增加了CCR7 mRNA的转录和MM-1细胞对CCL19/21的迁移能力。此外，我们的研究结果表明，在LXRα激活过程中，MM-1细胞上存在的e -前列腺素2和4 (EP2/EP4)受体的参与是观察到的CCR7 mRNA表达和功能增加的原因。检查单核细胞对慢性炎症部位产生的脂质衍生物(如PGE2和氧甾醇)的迁移反应，将有助于理解动脉粥样硬化特征的过度单核细胞迁移。

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引用次数: 3