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1.
本文报告感染构端螺旋体的豚鼠及正常豚鼠血清补体50%溶血(CH50)及血清对中性粒细胞(PMN)的趋化作用。结果显示感染组CH50明显降低,血清对PMN的趋化能力明显提高(P<0.01);经青霉素治疗后补体活性无明显改变(P>0.05)。提示补体系统参与了抗钧端螺旋体的感染,并对变态反应的免疫病理损伤有一定作用。  相似文献   

2.
目的:探讨p38MAPK信号传导通路阻断剂(CNI-1493)对大鼠重症急性胰腺炎(severe acute pancreatitis SAP)时外周血多形核粒细胞(polymorphonuclear,PMN)功能影响,方法:以胰胆管逆行注射5%牛磺胆酸钠建立SD大鼠SAP模型,将54只SD大鼠随机分为3组:假手术组(SO,n=18);SAP组(SAPn=18);CNI-1493治疗组(CNI,n=18),术后3h,6h,12h取血,用密度梯度法分离PMN,用流式细胞仪测定呼吸爆发功能,并测定PMN释放髓过氧化物酶(MPO)的变化情况。结果:SAP组PMN呼吸爆发亢进,MPO释放明显增加,在各时间点上CNI-1493都能抑制PMN的功能亢进,减少MPO的释放,结论:CNI-1493可以明显抑制SAP时PMN的病理性功能亢进,是治疗SAP的重要机制之一,提示可能具有临床应用的前景。  相似文献   

3.
1 中性粒细胞的生物学作用。中性粒细胞(PMN)是从骨髓中造血干细胞增殖分化而产生的,它的生成过程中,根据功能和形态特点,人为的划分为干细胞池、生长成熟池和功能池三个阶段.前两个阶段是在骨髓中增殖分化,粒细胞成熟后从骨髓释放至外周就进入功能池.感染、炎症、组织损伤等可致PMN向病灶部位渗出.PMN具有趋化作用、变形和黏附作用、吞噬和杀菌作用等功能,在机体防御和抵抗病原体侵袭过程中起重要的作用.炎症反应时,PMN在多种趋化因子的作用下呈阿米巴样运动,穿过毛细血管壁到达炎症部位,发挥生物学效应.然而,大量的PMN在组织中渗出却导致组织局部损伤.PMN作为一种需氧杀菌剂在执行其功能时可释放大量活性氧(ROS)和单态氧,产生呼吸爆发,引起进一步炎症反应.正常情况下,随着炎症的好转,渗出的PMN逐渐凋亡并被吞噬细胞吞噬.PMN的渗出和及时凋亡既有利于病原微生物的清除,又不至于对组织造成伤害。  相似文献   

4.
氟化物对人多形核白细胞SOD活力变化的影响   总被引:10,自引:3,他引:7  
目的 通过测定超氧化物歧化酶(SOD)活力变化,观察刀豆蛋白A(ConA)及与NaF对多形核中性粒细胞(PMN)超氧阴离子自由基(  相似文献   

5.
卢水华 《临床肺科杂志》2009,14(11):1505-1506
病原体感染时,为了有效地清除侵入肺脏和机体其他组织中的病原菌,特异性效应细胞必须聚集到感染部位,并与感染部位的病原菌发生相互作用。先天性免疫应答由定居在组织中的巨噬细胞和由血流移行到感染部位的中心粒细胞(PMN)和单核细胞(MN)完成;获得性免疫应答由感染局部的活化巨噬细胞、特异性抗原T细胞和B细胞完成。  相似文献   

6.
目的检测结核病患者外周血中性粒细胞(PMN)体外感染结核分枝杆菌(M.tb)前后L选择素(CD62L)的表达情况,并探讨CD62L在结核病的发展过程中的作用。方法应用流式细胞术检测结核病患者PMN表面CD62L的表达,同时检测正常人PMN的CD62L表达率;体外感染M.tb后,再检测结核病患者和正常人PMN的CD62L表达率。结果结核病患者PMN表面高表达CD62L,与正常人PMN表面CD62L表达无明显差异;感染M.tb后,结核病患者和正常人PMN表面CD62L表达率显著降低(P0.05)。结论结核病患者PMN表面CD62L参与了PMN的趋化过程,在结核炎症反应中发挥重要作用,推动结核病的发展过程。  相似文献   

7.
盐酸戊乙奎醚对内毒素致急性肺损伤的保护作用   总被引:12,自引:0,他引:12  
盐酸戊乙奎醚(penehyclidine hydrochloride,PHC)是中国原创的新型选择性的莨菪类药物。近来研究发现,其能改善微循环、降低毛细血管壁的通透性,具有细胞保护和减少溶酶体释放等作用。我们通过观察PHC对急性肺损伤(ALI)大鼠中性粒细胞(PMN)在肺脏聚集、脂质过氧化损伤、肺通透性和气体交换能力的影响,以探讨其保护作用及机制。  相似文献   

8.
目的探讨香烟烟雾提取物(CSE)诱导作用对人内皮细胞细胞间黏附分子-1(ICAM—1)和白介素-8(IL-8)表达以及与多形核中性粒细胞(PMN)黏附的影响。方法培养人脐静脉内皮细胞株(ECV-304);制备香烟烟雾提取物(CSE);用不同浓度(0、2.5%、5.0%、10.0%)CSE刺激内皮细胞,酶联免疫吸附测定(ELISA)法检测不同时间点(1h、3h、6h、9h、12h、24h、48h)收集的细胞培养上清液IL-8的浓度,细胞免疫化学染色(SABC)检测ICAM-1在不同时间点(3h、6h、9h、12h)内皮细胞上的表达,细胞记数法测定(1h、3h、6h、9h、12h)后PMN与内皮细胞的黏附率(PMN—EC)。结果(1)各CSE浓度组干预12h后,ICAM-1在EC上的表达量随着干预浓度的增加而增高,除了2.5%CSE干预组和5.0%CSE干预组之间无差异外,各组间差异均有非常显著性意义(P〈0.01);10.0%CSE干预不同时间点后,随着干预时间的延长,ICAM-1在内皮细胞上的表达量增加。各时间组之间差异均有非常显著性意义(P〈0.01)。(2)随着CSE干预浓度的增加和干预时间的延长,内皮细胞表达IL-8的浓度增高,各组间差异均有非常显著性意义(P〈0.01)。(3)各CSE浓度组干预12h后,PMN—EC黏附率随着干预浓度的增加而增加,各组间差异均有非常显著性意义(P〈0.01)。10.0%CSE干预不同时间点后,随着干预时间的延长,PMN—EC黏附率增加,各时间组差异均有非常显著性意义(P〈0.01)。结论香烟烟雾提取物可以刺激激活血管内皮细胞ICAM-1和IL-8表达,增强PMN与内皮细胞的黏附。  相似文献   

9.
1中性粒细胞的生物学作用中性粒细胞(PMN)是从骨髓中造血干细胞增殖分化而产生的,它的生成过程中,根据功能和形态特点,人为的划分为干细胞池、生长成熟池和功能池三个阶段。前两个阶段是在骨髓中增殖分化,粒细胞成熟后从骨髓释放至外周就进入功能池。感染、炎症、组织损伤等可致PMN向病灶部位渗出。PMN具有趋化作用、变形和黏附作用、吞噬和杀菌作用等功能,在机体防御和抵抗病原体侵袭过程中起重要的作用。炎症反应时,PMN在多种趋化因子的作用下呈阿米巴样运动,穿过毛细血管壁到达炎症部位,发挥生物学效应。然而,大量的PMN在组织中渗…  相似文献   

10.
目的研究急性心肌梗死(AMI)后患者血清粒细胞-巨噬细胞集落刺激因子(GM-CSF)水平变化,及其与心功能的关系。方法AMI患者30例,AMI后8,16,24,36,48 h及3,4,5,6,7 d分别测定血清GM-CSF,肌酸激酶同工酶(CK-MB)浓度。并在AMI 1周后测量左室射血分数(LVEF),左室舒张末期内径(LVEDD)。从30例患者中选取5例急性广泛前壁心梗,并且LVEF<40%的患者作为亚组,描述心梗后GM-CSF时间相;并分析30例患者血清GM-CSF峰值与心梗后心功能的关系。结果GM-CSF在AMI后8 h开始逐渐升高,3672 h达高峰,在以后7 d的测量中均保持较高水平。GM-CSF峰值与CK-MB峰值呈正相关(r=0.566,P<0.05);与LVEF呈负相关(r=-0.42,P<0.05);与LVEDD呈正相关(r=0.454,P<0.05)。结论心肌梗死后血清GM-CSF水平增高与心功能呈负相关。  相似文献   

11.
An accelerated model of human immunodeficiency virus central nervous system disease was developed in which more than 90% of infected macaques develop typical simian immunodeficiency virus (SIV) encephalitis with neuronal dysfunction by postinoculation (pi) day 84. Infected macaques had replicating virus and microglial activation in the brain 10 days after inoculation; viral replication and microglial activation were suppressed at pi day 21. By pi day 56, viral recrudescence in the brain was detected in 2 of 6 infected macaques. CD4 cells were the predominant lymphocytes in the brain during acute and asymptomatic infection; cytotoxic T lymphocytes and NK cells predominated in macaques with encephalitis. Low levels of peripheral blood NK lytic activity at pi day 10, elevated cerebrospinal fluid (CSF) monocyte chemoattractant protein-1 after 28 days, and high CSF viral RNA after 42 days predicted SIV encephalitis. This model is ideal to track the viral, cellular, and immunologic changes in the brain during acute and asymptomatic infection and during viral recrudescence and SIV encephalitis.  相似文献   

12.
BACKGROUND: Little is known about secretory immunity-the major defence mechanism at mucosal surfaces-in human immunodeficiency virus (HIV) infected patients, especially in the early stages of the disease. AIMS: The aim of the study was to analyse mucosal immunoglobulin production and simian immunodeficiency virus (SIV) specific antibody response in the intestinal mucosa during the course of SIV infection in comparison with serum and saliva. ANIMALS AND METHODS: IgG, IgA, and IgM concentrations were determined in supernatants of short term cultured duodenal biopsies, serum, and saliva from SIV infected rhesus macaques (n=8) and controls (n=2) by ELISA at defined times before and after infection. Specific antibodies to SIV were detected by western blot and/or dot blot analysis. In addition, rectal swabs from two uninfected and 12 SIV infected rhesus macaques (seven without and five with enteritis) were analysed for albumin and IgG concentrations. RESULTS: An increase in total intestinal IgG and a decrease in IgA were observed. SIV specific IgG or IgA responses were detectable as early as one week after SIV infection in the serum of seven of eight animals. In contrast, intestinal SIV specific IgG production was detected only four weeks after infection in six of eight animals, and intestinal SIV specific IgA was not produced in the intestine at any time point. In saliva, the secretory component on SIV specific IgA was only detected in one animal at week 24 after infection. Enteritis is frequent in SIV infected animals and results in a significant increase in albumin and IgG secretion into the intestinal lumen. CONCLUSION: Despite modest quantitative changes in mucosal immunglobulin production there was a total lack of SIV specific IgA synthesis in the intestine during SIV infection. This lack or disturbed secretory SIV specific IgA response at mucosal surfaces may explain the rapid and high HIV/SIV replication in this compartment. In addition, our investigations indicate secretion of serum proteins into intestinal fluids during SIV infection. Previous investigations using intestinal secretions or swabs for analysing quantitative and specific immunglobulins therefore should be interpreted with caution.  相似文献   

13.
The env polyprotein sequences of several simian immunodeficiency virus (SIV) isolates were analyzed using computer algorithms designed to predict immunologically reactive protein segments. Peptides corresponding to predicted epitopes were synthesized and employed in peptide enzyme-linked immunosorbent assay (ELISA) screening of serum panels from experimentally infected macaques, as well as naturally infected, asymptomatic mangabeys and African green monkeys. Several of the peptides are recognized by a high percentage of antisera from each panel of monkeys indicating that they represent group-specific antigenic determinants of SIV. Several type-specific determinants also were identified. These peptides may be a useful tool for studying the kinetics of SIV glycoprotein-specific immune responses produced by infected and vaccine-protected monkeys at the epitope level.  相似文献   

14.
15.
Abstract: Marrow stromal cells of patients treated by autologous bone marrow transplantation (ABMT) for malignancies have been assessed for their ability to secrete granulocyte colony-stimulating factor (G–CSF), granulocyte-macrophage colony-stimulating factor (GM–CSF), stem cell factor (SCF), leukemia inhibitory factor (LIF), interleukin-6 (IL-6), transforming growth factor β1 (TGFβ1) and macrophage inflammatory protein-1α (MIP-1α). Long-term marrow cultures were established from 10 patients prior to and 3 months after ABMT, from 7 patients 1 yr after ABMT and from 11 controls. Cytokines in culture supernatants of stromal layers (SL) were evaluated by enzyme-linked immunosorbent assay (ELISA). Significant differences between patient groups and controls were apparent in baseline production of GM–CSF, SCF, MlP-1α and TGFβ1. After IL-1β addition in cultures, G–CSF production was reduced in pretransplant and post-transplant patients compared to controls. The production of TGFβ1, LIF, IL-6 and more particularly SCF were reduced in post-transplant patients, while elevated levels of GM–CSF and MIP-1α were observed in these patients only when the values were corrected for the number of cells growing in the SL. These results indicate a prolonged stromal defect in growth factor production following ABMT for the early-stage acting cytokines IL-6, LIF and SCF as well as for G–CSF, but not for GM–CSF, while the production of the 2 inhibitors shows different pathways.  相似文献   

16.
F Colotta  F Re  N Polentarutti  S Sozzani  A Mantovani 《Blood》1992,80(8):2012-2020
Mature circulating polymorphonuclear cells (PMN) have the shortest half-life among leukocytes and undergo rapid programmed cell death in vitro. In this study, we have examined the possibility that inflammatory signals (cytokines and bacterial products) can regulate PMN survival. PMN in culture were found to rapidly die, with percentages of survival at 24, 48, 72, and 96 hours of 97.3% +/- 1.9%, 36.8% +/- 5.3%, 14.5% +/- 3.1%, and 4.2% +/- 2.9%, respectively (mean +/- SE of 20 different donors). PMN incubated with interleukin-1 beta (IL-1 beta), tumor necrosis factor, granulocyte-macrophage colony-stimulating factor (CSF), granulocyte-CSF, and interferon-gamma (IFN-gamma), but not with prototypic chemoattractants (fMLP, recombinant C5a, and IL-8), showed a marked increase in survival, with values ranging at 72 hours of incubation from 89.5% +/- 5.8% for IL-1 beta to 47.6% +/- 6.4% for IFN-gamma. The calculated half-life was 35 hours for untreated and 115 hours for IL-1-treated PMN. PMN activated with lipopolysaccharide (LPS) or inactivated streptococci also showed a longer survival compared with untreated cells (94.4% +/- 3.2% and 95.5% +/- 2.4%, respectively, at 72 hours). PMN surviving in response to LPS or IL-1 beta retained the capacity to produce superoxide anion when treated with phorbol esters or fMLP. All inducers of PMN survival protect these cells from programmed cell death because they reduced cells with morphologic features of apoptosis and the fragmentation of DNA in multiples of 180 bp. Thus, certain cytokines and bacterial products can prolong PMN survival by interfering with the physiologic process of apoptosis. Prolongation of survival may be important for the regulation of host resistance and inflammation, and may represent a crucial permissive step for certain cytokines and microbial products that activate gene expression and function in PMN.  相似文献   

17.
目的探讨粒细胞-巨噬细胞集落刺激因子(GM-CSF)在哮喘嗜酸细胞(Eos)炎症中的作用。方法建立哮喘豚鼠实验模型,用雷公藤处理,观察肺组织Eos密度,斑点分子杂交检测支气管肺组织GM-CSFmRNA含量。结果哮喘组肺组织Eos浸润密度增加,GM-CSFmRNA表达水平增高,与对照组相比差异有显著性(P<0.05)。雷公藤处理后mRNA表达显著降低,但Eos浸润密度减少不明显。结论GM-CSFmRNA表达增加可能是导致哮喘Eos气道炎症的原因。雷公藤能抑制GM-CSFmRNA表达,可能具有哮喘抗炎治疗的潜在应用价值。  相似文献   

18.
粒-巨噬细胞集落刺激因子在肺泡蛋白沉积症患者中的表达   总被引:13,自引:0,他引:13  
目的 研究粒-巨噬细胞集落刺激因子(GM-CSF)蛋白及mRNA在4例肺泡蛋白沉积症(PAP)患者中的表达,探索PAP的发病机制。方法 采用ELISA法测定GM-CSF蛋白,采用RT-PCR检测外周血单个核细胞及肺泡巨噬细胞中GM-CSFmRNA表达水平。GM-CSFcDNA测序采用双脱氧链终止反应法。结果 4例PAP中3例外周血单个核细胞和肺泡巨噬细胞均检测不到GM-CSF释放,但mRNA表达水平均正常。cDNA测序发现1例PAP患者GM-CSFcDNA第382位碱基发生点突变(T→C),致117位氨基酸序列发生改变(异亮氨酸→苏氨酸)。结论 GM-CSF蛋白表达异常与PAP发病可能有关,GM-CSFcDNA点突变可能是导致GM-CSF蛋白表达异常的原因之一。  相似文献   

19.
Cerebrospinal fluid (CSF) samples were collected from 24 uninfected and 24 SIV251 MPBMC-infected rhesus monkeys during early infection and from 6 animals in a longitudinal design up to 7 months postinfection to investigate excitatory and inhibitory amino acid neurotransmitter levels. During the early infection period CSF amino acid concentrations of infected animals were not significantly different from those of uninfected animals. However, long-term studies demonstrated that gamma-aminobutyric acid (GABA) concentrations were decreased while glutamate concentrations were increased late in infection compared with the preinfection values of the same animals. Moreover, we showed that the source of increased glutamate in animals with AIDS is, at least partially, microglial cells. Our data support the hypothesis that excitotoxicity is involved in immunodeficiency virus-induced neurological disease and propose microglia as a contributor to excitotoxic damage.  相似文献   

20.
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