单核细胞趋化蛋白-1与口腔疾病关系的研究进展

单核细胞趋化蛋白-1是趋化因子CC亚族成员之一,能趋化和激活单核细胞、巨噬细胞等,参与调节多种生理、病理和免疫应答过程。下面就单核细胞趋化蛋白-1的结构及其与口腔常见疾病,如牙髓炎、根尖周炎、牙周炎和口腔鳞癌等的关系作一综述。     

白细胞介素-1β对人牙周膜成纤维细胞中MCP-1表达影响的研究

目的:探讨白细胞介素-1β(IL-1β)对人牙周膜成纤维细胞(hPDLFs)中单核细胞趋化蛋白-1(MCP-1)表达水平的影响。方法:体外分离培养的人牙周膜成纤维细胞随机分为实验组和对照组,实验组细胞以不同浓度IL-1β(1、5、10、25 ng/mL)作用24 h;对照组细胞则不加IL-1β作用。分别采用半定量逆转录聚合酶链反应(RT-PCR)检测人牙周膜成纤维细胞中MCP-1 mRNA的表达;采用免疫荧光技术观察MCP-1的表达情况;采用Western blot方法检测其蛋白表达变化。结果:对照组hPDLFs中可见微弱的MCP-1表达;实验组hPDLFs经IL-1β刺激后,MCP-1在mRNA和蛋白水平表达都增强,这种调节作用在10 ng/mL IL-1β的作用浓度时最明显(P<0.05)。结论:在IL-1β介导环境下,hPDLFs中MCP-1的表达增高,而MCP-1表达增高可能是引起外周血单核细胞向局部炎症牙周组织募集的机制之一。     

单核细胞趋化蛋白-1和细胞间黏附分子-1与动脉粥样硬化和牙周病的关系

以动脉粥样硬化为病理基础的冠心病是目前主要的致死性疾病之一,而牙周病与动脉粥样硬化之间存在着一定的相关性。单核细胞趋化蛋白(MCP)-1和细胞间黏附分子(ICAM)-1在动脉粥样硬化和牙周病的发生发展中起着重要的作用。本文就MCP-1和ICAM-1以及二者与动脉粥样硬化、牙周病间的关系作一综述。     

单核细胞趋化蛋白-1和细胞间黏附分子-1与动脉粥样硬化和牙周病的关系

以动脉粥样硬化为病理基础的冠心病是目前主要的致死性疾病之一，而牙周病与动脉粥样硬化之间存在着一定的相关性。单核细胞趋化蛋白（MCP）-1和细胞间黏附分子（ICAM）-1在动脉粥样硬化和牙周病的发生发展中起着重要的作用。本文就MCP-1和ICAM-1以及二者与动脉粥样硬化、牙周病间的关系作一综述。     

表皮生长因子对大鼠牙囊细胞单核细胞趋化蛋白-1表达的影响

目的:研究表皮生长因子(EGF)对体外培养的大鼠牙囊细胞单核细胞趋化蛋白-1(MCP-1)表达的影响.方法:原代培养Wistar大鼠牙囊细胞,选择生长良好的第3代细胞,分别加入不同浓度的EGF与牙囊细胞共孵育5d,MTT法对比观察不同浓度的EGF对牙囊细胞增殖活性的影响,筛选EGF作用于牙囊细胞的最佳效应浓度.将第3代牙囊细胞以1×105/孔接种到培养皿中,加入最佳浓度的EGF孵育0、0.5、1、3、6h后,Trizol一步法分别提取总RNA,采用反转录聚合酶链反应(RT-PCR)检测同一浓度的EGF作用不同时间后,牙囊细胞MCP-1 mRNA的表达变化.数据采用SPSS13.0软件包进行方差分析.结果:在EGF浓度为5～10 ng/ml时,牙囊细胞的增殖活性显著增高(P＜0.05),10 ng/ml时达到最高(P＜0.01).牙囊细胞与10ng/ml的EGF共同孵育3 h,MCP-1 mRNA表达最高(P＜0.01),以后逐渐恢复,但仍比对照组高(P＜0.05).结论:EGF与其受体结合,可作用于牙囊细胞,适当浓度的EGF能显著增加牙囊细胞的增殖活性,并且EGF可通过上调牙囊细胞中MCP-1 mRNA的表达.促进单核细胞聚集.调节牙的萌出.     

白细胞介素-1基因与牙周炎和冠心病相关性研究进展

流行病学研究显示,牙周炎和冠心病的发病明显相关。近年来,国内外研究发现,炎症性细胞因子——白细胞介素-1(IL-1)基因多态性与慢性牙周炎和冠心病的易感性明显相关。本文就IL-1基因与牙周炎和冠心病的关系作一综述。     

慢性牙周炎牙周基础治疗前后血清超敏C反应蛋白与单核细胞趋化蛋白-1变化研究

目的    研究慢性牙周炎对血清超敏C反应蛋白（hs-CRP）和单核细胞趋化蛋白-1（MCP-1）浓度的影响。方法    选取2015—2016年于中国人民解放军陆军总医院口腔科门诊就诊的80例牙周炎患者（牙周病组）和40名无牙周炎症状的志愿者（对照组）。初诊记录探诊出血（BOP）、牙周探诊深度（PD）和临床附着丧失（CAL）情况,收集空腹静脉血,检测血清超敏C反应蛋白（hs-CRP）和单核细胞趋化蛋白-1（MCP-1）。对牙周病组进行为期3个月的牙周基础治疗,治疗结束3个月后,再次收集空腹静脉血,检测血清hs-CRP和MCP-1。结果    牙周病组与对照组基线条件无明显差异。对照组hs-CRP和MCP-1浓度为（1.48 ± 1.1）mg/L和（42.3 ± 4.9）mg/L,牙周病组分别为（3.89 ± 2.8）mg/L和（88.7 ± 5.8）mg/L,两组差异有统计学意义（P＜0.05）。牙周治疗结束3个月后,牙周病组hs-CRP和MCP-1浓度为（2.04 ± 1.5）mg/L和（64.2 ± 5.1）mg/L,与治疗前比较差异有统计学意义（P＜0.05）。结论    　慢性牙周炎可引起低滴度菌血症,造成血清炎症标志物hs-CRP和MCP-1浓度增高,有效的牙周基础治疗可降低血清hs-CRP和MCP-1。     

白细胞介素- 8对牙周炎易感性的作用研究进展

白细胞介素-8(interleukin-8,IL-8)是一种中性粒细胞功能调节因子,对牙周炎的发生、发展具有重要影响.而牙周炎在一定程度上表现出明显的宿主易感性,与遗传基因关系密切.从基因水平研究IL-8对牙周炎易感性的作用有助于牙周炎的预防和早期控制.笔者从IL-8的基因结构、表达、致炎机制等方面对其在牙周炎遗传易感...     

白细胞介素-8对牙周炎易感性的作用研究进展

白细胞介素-8（interleukin-8,IL-8）是一种中性粒细胞功能调节因子,对牙周炎的发生、发展具有重要影响。而牙周炎在一定程度上表现出明显的宿主易感性,与遗传基因关系密切。从基因水平研究IL-8对牙周炎易感性的作用有助于牙周炎的预防和早期控制。笔者从IL-8的基因结构、表达、致炎机制等方面对其在牙周炎遗传易感性中的作用进行综述。     

白细胞介素-1与牙槽骨的改建

白细胞介素 - 1(IL - 1)是一种具有多种生物学活性的细胞因子 ,在骨的代谢中起着重要的作用。由于口腔的特殊环境 ,牙槽骨总是受到力的作用。本文就 IL- 1对骨的改建 ,力对牙槽骨的改建以及 IL- 1、力与牙槽骨改建的关系作一综述。     

Role of substance P and calcitonin gene-related peptide in the regulation of interleukin-8 and monocyte chemotactic protein-1 expression in human dental pulp

AIM: To determine whether leucocyte infiltration during neurogenic inflammation in the pulp is regulated by neuropeptides via inducing the release of proinflammatory chemokines interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1) from human dental pulp. METHODOLOGY: Cultured primary pulp cells and pulp tissue explants were stimulated with substance P (SP) and/or calcitonin gene-related peptide (CGRP). IL-8 or MCP-1, secreted from cultured cells or produced in pulp explants, was analysed by enzyme-linked immunosorbent assay. RESULTS: Substance P induced IL-8 secretion from cultured pulp cells (approximately threefold increase over control, P < 0.05) and from pulp tissue explants (two- to three fold). SP only minimally to moderately induced MCP-1 (approximately two fold) in cultured pulp cells. While MCP-1 induction in cultured pulp cells was detected after 24 h of SP stimulation, no induction was observed in pulp tissue. CGRP did not induce IL-8, but moderately increased MCP-1 production (approximately three fold) in cultured pulp cells. There was no synergistic induction of MCP-1 by SP plus CGRP stimulation of pulp cells. CONCLUSIONS: Substance P is a stronger inducer of IL-8 production in dental pulp than CGRP. IL-8 is more strongly induced than MCP-1 by SP, suggesting a more important role for IL-8 than MCP-1 in leucocyte infiltration during neurogenic inflammation in dental pulp.     

CD40在人炎症牙髓组织中的表达

目的：探讨在牙髓炎中CD40的表达,揭示CD40在牙髓炎发生发展中的可能作用。方法：采用免疫组织化学的方法检测人的正常及急、慢性牙髓炎牙髓中CD40的表达。结果：免疫组化染色观察正常牙髓组织中,CD40未见阳性表达,而在急慢性牙髓炎组织中CD40在浆细胞、巨噬细胞上有不同程度的表达。慢性牙髓炎组表达明显强于急性牙髓炎组。结论：CD40在牙髓炎牙髓组织中呈阳性表达,CD40参与了牙髓的炎症反应。     

Altered CD40 and E-cadherin expression – putative role in oral lichen planus

BACKGROUND: Oral lichen planus (OLP) is characterized among other features by apoptosis of basal keratinocytes. To identify potential regulatory mechanisms associated with basal cell apoptosis in OLP, we investigated the expression of CD40, CD40 ligand (CD40L), CD44 and epithelial (E)-cadherin. METHODS: Biopsies from 22 patients with OLP were investigated by immunohistochemistry for detection of CD40, CD40L, E-cadherin, CD44, Laminin-5 and Collagen IV, double-labelling for CD40 and CD3, and in situ mRNA hybridization for CD40 and CD40L. RESULTS: In actively diseased areas of OLP lesions, basal keratinocytes did not express CD40 and were focally E-cadherin-negative, in contrast to non-diseased areas and normal oral mucosa. Demonstration of intraepithelial T cells expressing CD40 and CD40L, indicates a potential role in inflammatory cell responses involved in the disease process of OLP. CONCLUSION: T cells may orchestrate inflammatory cell responses in OLP via CD40-CD40L interactions. As basal keratinocytes downregulate CD40, they may escape CD40-CD40L-induced apoptosis in OLP. On the other hand, loss of E-cadherin expression may contribute to epithelial basal cell destruction and T-cell migration into the epithelial compartment in OLP.     

The immunohistology of CD40 in human oral epithelium in health and disease

BACKGROUND: CD40 has a role in the regulation of immune responses, cell proliferation and migration, and apoptosis. Little is known of its distribution in oral mucosal pathology. METHODS: Oral keratinocyte lines were tested for CD40 protein by Western blotting. Immunohistochemistry was used to stain paraffin sections of oral mucosa in health and in inflammatory, reactive, dysplastic and malignant disease. RESULTS: Western blotting confirmed the presence of CD40 in oral keratinocytes. CD40 was generally expressed by keratinocytes in the basal layer, with variable parabasal expression. Langerhans cells also stained positively. Expression was lost in nine of 33 (27%) epithelial dysplasias, seven of which were severe. Eighty-one percent of well, 69% of moderately and 50% of poorly differentiated oral squamous cell carcinomas (OSCC) expressed CD40. Overall, 45 of 65 (69%) OSCC were positive. The pattern of expression was unrelated to tumour differentiation. CONCLUSION: CD40 expression by basal and parabasal oral keratinocytes is physiological. Expression is lost in approximately one-third of oral epithelial dysplasias and OSCC. The significance of such loss remains unknown, but may be related to immunological or other abnormalities of keratinocyte homeostasis.     

Differential in situ distribution of interleukin-8, monocyte chemoattractant protein-1 and Rantes in human chronic periapical granuloma

In situ distribution of three prototype chemokines interleukin (IL)-8, monocyte chemoattractant protein (MCP)-1 and Rantes was determined in chronic human periapical granulomas by immunohistochemistry using monoclonal antibodies. IL-8 was found primarily in the cytoplasm of the Malassez epithelial cells. MCP-1 immunoreactivity was confined to the endothelial cells that lined small venules. Each of the three investigated chemokines, including Rantes, exhibited a characteristic binding pattern to the extracellular matrix of the lesion. The observed chemokines may play a role in establishing the cellular composition of chronic apical periodontitis, thus augmenting the intensity of local inflammation and tissue damage.     

单核细胞趋化蛋白-1在种植体周围组织中的表达

目的：研究单核细胞趋化蛋白-1在不同种植体周围软组织和骨组织中的表达变化。方法：选用8只健康成年杂种狗,拔除双侧下颌第一、二、三前磨牙,3月后植入种植体。采用丝线结扎法建立狗实验性种植体周围炎模型,分别在丝线结扎后1周、2月和6月时处死实验动物,处死动物前记录牙周袋深度（PPD）、菌斑指数（PI）和改良龈沟出血指数（MBI）,根据种植体周围炎症情况分健康组、炎症组和种植失败组。取种植体周围软组织用半定量RT-PCR法检测MCP-1 mRNA的表达,取种植体周围骨组织进行免疫组化染色,检测MCP-1的表达情况。用SPSS软件分析不同组别和不同时间点种植体周围软组织和骨组织中MCP-1的表达差异。结果：种植体周围软组织中MCP-1 mRNA的相对表达量在健康组较低（0．11±0．02）,显著低于炎症组（0．24±0．05）和种植失败组（0．29±0．04）,但炎症组和种植失败组无差别。实验组种植体1周MCP-1 mRNA的相对表达量开始增加,显著高于对照组,1月时最高,但2月和6月时无明显差异。种植体周围骨组织中MCP-1的累积光密度值在健康组（412．36±42．11）低于炎症组（1134．89±56．47）和种植失败组（1345．65±46．23）,实验组种植体MCP-1的表达从基点后2月开始增加,对照组无明显变化。结论：MCP-1在种植体周围软组织和骨组织中均有表达,但变化不同步;MCP-1能反映种植体周围软组织的炎症状况,但与种植体周围骨吸收的关系还需进一步研究。     

牙髓卟啉单胞菌脂多糖对小鼠成骨细胞表达MCP-1的影响

目的: 探讨牙髓卟啉单胞菌(Porphyromonas endodontalis,P.endodontalis)脂多糖对小鼠成骨细胞表达单核细胞趋化蛋白1(monocyte chemotactic protein-1, MCP-1)mRNA和蛋白的影响,以及是否有p38丝裂原活化蛋白激酶（mitogen-activated protein kinase,MAPK）信号通路和核因子κB（Nuclear Factor-κB, NF-κB）信号通路的参与。方法: 以不同质量浓度的P.endodontalis脂多糖(0~50 mg/L)刺激MC3T3-E1细胞24 h;以20 mg/L P.endodontalis脂多糖作用于细胞不同时间（0~48 h）后,采用实时反转录PCR和酶联免疫吸附测定检测MCP-1mRNA和蛋白的表达。采用p38MAPK抑制剂SB203580和NF-κB抑制剂BAY11-7082分别预处理细胞1 h,检测其对P.endodontalis脂多糖刺激MC3T3-E1细胞后MCP-1mRNA表达的影响。采用SPSS 13.0软件包对结果进行单因素方差分析和Dunnett t检验。结果: 不同质量浓度的P.endodontalis脂多糖（0~50 mg/L）刺激MC3T3-E1细胞后,MCP-1的mRNA表达和蛋白分泌呈剂量依赖性;观察时间内（0~48 h）,20 mg/L P.endodontalis脂多糖作用于MC3T3-E1细胞后,MCP-1 mRNA的表达和蛋白分泌呈时间依赖性;10 mol/L的SB203580和BAY11-7082分别预处理细胞1 h,可以降低P.endodontalis脂多糖诱导MCP-1 mRNA的表达,且SB203580的抑制作用强于BAY11-7082。结论: P.endodontalis脂多糖可能通过激活p38MAPK和NF-κB信号通路诱导成骨细胞表达MCP-1mRNA和蛋白。