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Cellular subsets of the milky spots in the human greater omentum   总被引:11,自引:0,他引:11  
Summary The cellular composition of the human milky spots was investigated on surgically removed specimens of the greater omentum of three 8-month-old infants operated on for neuroblastoma. Monoclonal antibodies and immunohistochemical methods for recognition of macrophages, B-lymphocytes and T-lymphocytes and toluidine-blue staining for mast cells were used. The mean number of cells in one milky spot amounted to 570±33. This cell population was composed of 47.5% macrophages, 29.1% B-lymphocytes, 11.7% T-lymphocytes and 6.1% mast cells. Since inflammation was absent in the material investigated, the numerical data found in the present paper could be regarded as representative cell levels of normal milky spots.  相似文献
Protease-activated receptors (PARs) belong to a family of G-coupled seven transmembrane receptors that are activated by a proteolytic cleavage of their N-termini. Recent studies suggest the involvement of protease-activated receptors-1 and -2 (PAR-1, PAR-2) activators in mast cell de-granulation in various physiological and pathophysiological processes in inflammatory responses. Although PAR-1 and PAR-2 activating proteases, thrombin and tryptase, have been associated with mast cell activation, PAR-1 and PAR-2 have not been localized within these cells. We describe here the localization of PAR-1 and PAR-2 in mast cells from various normal human tissues using im-munohistochemical and double immunofluorescence techniques. The presence of these receptors on the membrane may explain the actions of accessible extracellular thrombin and tryptase for mast cell activation. In addition to the membrane labeling, these receptors are also localized on the membrane of the intracellular tryptase-positive granules, which may function to sustain further mast cell degranulation upon exocytosis. The localization of these two receptors in mast cells suggests a novel mechanism for controlling mast cell activation through regulation of PARI and PAR-2.  相似文献
Thrombin as a Regulator of Inflammation and Reparative Processes in Tissues   总被引:10,自引:0,他引:10  
Activation of blood coagulation and thrombin formation accompany inflammation, wound healing, atherogenesis, and other processes induced by endothelial injury. Systems of hemostasis and inflammation play an important role in the pathogenesis of acute coronary syndromes. This paper reviews thrombin functions involved in its interaction with PAR family receptors, activation of platelets, endothelial cells, leukocytes, smooth muscle cells, and mast cells. Mechanisms of regulatory effects of thrombin on mast cells associated with nitric oxide release are discussed.  相似文献
Transient increases of intracellular calcium and exocytotic activity of rat peritoneal mast cells following stimulation with compound 48/80 were monitored using the Ca-indicator dye fura-2 and the capacitance measurement technique. It is known that mast cells very rapidly lose their secretory response towards antigenic or compound 48/80-induced stimulation in the whole-cell recording configuration of the patch-clamp technique due to washout of signal mediators. In contrast, we found that calcium transients remained unaffected by intracellular dialysis for as long as 10 min.The fast washout phenomenon of exocytosis could be overcome by supplementing the pipette filling solution with guanosinetriphosphate (GTP) indicating a major role for GTP-binding proteins in secretion. The restoration of exocytosis was transient and decayed within three minutes, suggesting diffusional escape of one or several other cytoplasmic substances involved in stimulus-secretion coupling. Quantitative aspects of this process and the implications of its differential effects on Ca-transients versus secretion are discussed.  相似文献
He SH  Xie H  He YS 《生理学报》2002,54(6):531-534
研究反肉桂酰-亮-异亮-甘-精-亮-鸟-[酰胺](tc-LIGRLO),一种PAR-2激动剂,对肥大细胞类胰蛋白酶释放的影响。结果显示,经过15min的培养,tc-LIGRLO可引起比基础分泌量增加1倍以上的类胰蛋白酶释放,作用强度超过抗IgE抗体和钙离子导入剂(calcium ionophore A23187,CI),而反PAR-2激动剂-反肉桂酰-鸟-亮-精-甘-异亮-亮-[酰胺](tc-OLRGIL)无此作用,培养时间延长到30min时对tc-LIGRLO的作用无明显影响,其时间关系曲线表明,tc-LIGRLO的作用从1min开始,3min后达高峰,结果表明,PAR-2激动剂tc-LIGRLO是一种高效类胰蛋白酶释放刺激剂,在肥大细胞上可能有PAR-2存在。  相似文献
高原鼠兔肺动脉血管功能及形态变化   总被引:9,自引:1,他引:8  
目的研究肺循环对慢性缺氧的适应机理.方法在4300m的高度捕捉到高原适应动物鼠兔,带到2260m的高度并和10只Wistar大鼠在模拟4300m和5000m高度的低压仓内进行了肺动脉压的测定,观察肺组织学和组织免疫化学的改变.结果在2260m,鼠兔的Ppa明显低于Wistar大鼠,二者分别为(1.5±0@07)kPa和(2.9±1.1)kPa(P<0.01).随着海拔高度的增加,鼠兔的Ppa上升不明显,而Wistar大鼠增加显著.左右心室比重鼠兔为0.22,而Wistar大鼠为0.45.鼠兔的Hb,Hct和2.3-DPG均低于大鼠.大鼠肺小血管周围可见肥大细胞(7.1±0.33)mm2,免疫组化染色mastcelltyptase颗粒呈阳性,鼠兔未发现肥大细胞及此种免疫反应.肺小动脉中层较鼠兔厚,分别为27.21%和9.22%,壁的厚度和Ppa有很好的(r=0.763).结论鼠兔无低氧性肺血管收缩,是一种遗传性适应.大鼠肥大细胞通过激活某些生长因子,在肺血管的再建过程中可能起一定作用.  相似文献
新生大鼠雌激素注射后睾丸肥大细胞的变化   总被引:9,自引:0,他引:9  
新生大鼠注射雌二醇后,睾丸肥大细胞于第30天可见到,细胞数量随年龄增长而增多,生后4-6个月,睾丸网附近仍可见大量肥大细胞。睾丸内的肥大细胞比皮肤内的结缔组织肥大细胞(CTMC)小而与小肠粘膜的粘膜肥大细胞(MMC)相近,AB-S染色后基本着蓝色,硫酸小檗碱荧光染色后呈现中等强度黄色荧光,结果提示,新生大鼠雌激素注射后睾丸内肥大细胞的增多可能与免疫过程有关,睾丸内肥大细胞与CTMC和MMC皆有所不同。  相似文献
动情周期中大鼠子宫和输卵管壁肥大细胞数量变化的研究   总被引:8,自引:2,他引:6  
用放射免疫分析法对动情周期中大鼠血清雌二醇浓度进行检测;取子宫、输卵管常规石蜡切片、H-E染色,并用甲苯胺蓝染色显示肥大细胞,于光镜低倍视野下计数。结果显示:动物血清雌二醇浓度依次为:动情期(E)组>动情前期(PE)组>动情后期(ME)组>动情间(DE)且,各组间差异均有显性;在子宫,肥大细胞分布于宫壁肌怪平滑肌束间的结缔组织内、近小血管处,以微血管周居多,常见单个散在,于ME子宫内膜尚偶见肥大细胞;输卵管肥大细胞局限于其外膜层内、近小血管周围,亦多散在。子宫、输卵管壁内的肥大细胞镜下呈圆形、椭圆形或略不规则形,胞浆内充满紫红色粗大颗粒,子宫肥大细胞数量依次为:ME>DE>PE>E,各组间差异有生(DE与PE、PE与E,P<0.05,余组间P<0.01);输卵管壁内肥大细胞数量各组间差异无显性(P>0.05)。本尚对大鼠血清雌二醇水平波动与子宫、输卵管壁内肥大细胞数量变化的关系及其生理意义进行了讨论。  相似文献
Chymase released from activated mast cells induces apoptosis of vascular smooth muscle cells (SMCs) in vitro by degrading the pericellular matrix component fibronectin, so causing disruption of focal adhesion complexes and Akt dephosphorylation, which are necessary for cell adhesion and survival. However, the molecular mechanisms of chymase-mediated apoptosis downstream of Akt have remained elusive. Here, we show by means of RT-PCR, Western blotting, EMSA, immunocytochemistry and confocal microscopy, that chymase induces SMC apoptosis by disrupting NF-kappaB-mediated survival signaling. Following chymase treatment, the translocation of active NF-kappaB/p65 to the nucleus was partly abolished and the amount of nuclear p65 was reduced. Pretreatment of SMCs with chymase also inhibited LPS- and IL-1beta-induced nuclear translocation of p65. The chymase-induced degradation of p65 was mediated by active caspases. Loss of NF-kappaB-mediated transactivation resulted in downregulation of bcl-2 mRNA and protein expression, leading to mitochondrial swelling and release of cytochrome c. The apoptotic process involved activation of both caspase 9 and caspase 8. The results reveal that, by disrupting the NF-kappaB-mediated survival-signaling pathway, activated chymase-secreting mast cells can mediate apoptosis of cultured arterial SMCs. Since activated mast cells colocalize with apoptotic SMCs in vulnerable areas of human atherosclerotic plaques, they may participate in the weakening and rupture of atherosclerotic plaques.  相似文献
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