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排序方式: 共有622条查询结果,搜索用时 11 毫秒
1.
目的探讨温度、抗凝剂(EDTA-K2)对血嗜酸性粒细胞阳离子蛋白(ECP)水平的影响。方法采用固相双位点酶放大化学发光法,分别对22例健康体检者在两种不同温度(25℃和37℃)的血清标本,以及在相同温度(37℃)下,加抗凝剂和不加抗凝剂的血标本进行ECP水平测定。结果25℃组和37℃组血清ECP水平分别为8.92±6.45μg/L(x±s)和19.87±12.16μg/L(x±s),两组有显著性差异(P<0.01);37℃温度下加抗凝剂和不加抗凝剂血标本的ECP水平分别为5.26±2.60μg/L(x±s)和19.87±12.16μg/L(x±s),两组也有显著性差异(P<0.001)。结论温度和抗凝剂(EDTA-K2)对血标本的ECP水平测定有不同程度的影响。 相似文献
2.
Gü l Gü rsel Haluk Tü rktas Nahide G k ora Ishak
zel Tekin 《The Journal of asthma》1997,34(4):313-319
The aim of the present study was to investigate whether sputum eosinophil cationic protein (ECP) concentrations could be a useful marker in the differential diagnosis between intrinsic asthma and chronic obstructive pulmonary disease (COPD). For this purpose total blood eosinophil counts were obtained and concentrations of serum and sputum ECP from 10 nonatopic asthmatics with a mild attack and 9 COPD patients with acute exacerbation were measured by radioimmunoassay. Mean serum ECP concentration was 54.3 ± 23.0 g/L in the asthmatic group and 83.3 ± 79.2 g/L in the COPD group (p: n.s.). In the group of asthmatics mean sputum ECP level was 984.5 ± 1245.5 mg/L/g sputum and in the COPD group it was 417.5 ± 363.5 mg/L/g sputum. There was no significant difference in sputum ECP levels between patients with asthma and COPD. We conclude that neither sputum nor serum ECP levels are useful markers in differential diagnosis of asthma attack and acute exacerbation of COPD. 相似文献
3.
Substance P (SP) is a tachykinin involved in the regulation of inflammatory processes. To investigate a modulatory role of the neuropeptide SP in allergic inflammation, we studied its priming effect on human eosinophil chemotaxis and kinetic responses towards platelet activating factor (PAF) and recombinant human interleukin 5 (rhlL-5). Blood was obtained from normal subjects and eosinophils were separated by Percoll discontinuous density gradient centrifugation. High purification was obtained by negative selection procedure (CD16-beads) and the experiments were performed in a 48-well microchemotaxis Boyden chamber. In the present study we demonstrate a potent synergistic effect of 100nM dose of SP on the migratory function of human eosinophils stimulated by PAF and rhIL-5. This synergism was chemotaxis specific and was abolished by NK-1 receptor antagonist (FK888). The results suggest that neurogenic stimuli may play a significant role in eosinophil infiltration via its priming effect on the cell. 相似文献
4.
Wistar大鼠随机分3组,每天组予环磷酰胺组(CP)8mg/kg·d×4W,ip;冲击组予CP56mg/kg·d×4W,ip;对照组予生理盐水1ml/d×4W,ip。结果:①睾丸生精细胞损伤:每日组重于冲击组;②血睾酮(T)含量每日组显著低于冲击组(P<0.05);冲击组与对照组无显著差异(P>0.05)。③对睾丸间质细胞的影响:冲击组轻于每日组;④血FSH、LH含量与垂体重量:每日组与冲击组皆正常;⑤血BUN、Cr水平:3组皆正常.说明CP冲击疗法对睾丸间质细胞损伤较轻;CP除直接损伤睾丸组织外,可能还对下丘脑—垂体—睾丸轴有抑制作用. 相似文献
5.
Synergistic interactions between cytokines, chemokines and adhesion molecules may facilitate the selective recruitment of eosinophils into sites of allergic inflammation. Ovalbumin-sensitized IL5TG mice responded to antigen challenge with robust airway eosinophilia 24 and 72 hr post-exposure. Adhesion molecule expression and functional responsiveness of immune cells derived from IL5TG mice to various inflammatory mediators were evaluated. IL5TG-derived eosinophils, but not neutrophils, expressed higher levels of CD49d and CD11b relative to WT. Functional responsiveness to eotaxin was increased in IL5TG eosinophils as demonstrated by a 10× increase in its potency in producing actin polymerization and 3× increase in CD11b upregulation relative to WT. These data are consistent with increased CCR3 expression on IL5TG eosinophils. Responsiveness of eosinophils to LTB4 or MIP-1 was similar between WT and IL-5TG mice. These data provide evidence of synergy between eosinophil-specific cytokines and chemokines that may promote accumulation of this cell type under conditions of allergic inflammation in vivo. 相似文献
6.
Secretion of a chemotactic factor for neutrophils and eosinophils by alveolar macrophages from asthmatic patients 总被引:10,自引:0,他引:10
Philippe Gosset Ph.C. AndrBernard Tonnel M.D. Michel Joseph Ph.D. Lionel Prin M.D. Anne Mallart M.D. Jacques Charon D.D.S. Andr Capron M.D. 《The Journal of allergy and clinical immunology》1984,74(6):827-834
The studies presented in this article demonstrate the release of an IgE-dependent chemotactic factor for polymorphonuclear neutrophils (PMN) and eosinophils by alveolar macrophages (AMs) from normal subjects (n = 15) and allergic asthmatic patients (n = 15). A 60-minute incubation of normal AMs previously sensitized by 20% nonheated allergic sera with anti-human IgE antibody or the related allergen induced the release of a chemotactic activity (CA) for PMN and eosinophils in culture supernatants. When AMs were obtained from asthmatic patients, direct incubation with anti-IgE or the related allergen induced the same CA, whereas incubation with an unrelated allergen failed to produce CA (neutrophil CA after addition of anti-IgE, 22.5 +/- 3.5 cells per high power field; with related allergen, 15.8 +/- 3.6; with unrelated allergen, 0.7 +/- 1.8; p less than 0.0001). A partial characterization of the neutrophil chemotactic factor was carried out. Enzymatic treatment by trypsin or carboxypeptidase or by heating (56 degrees C for 3 hr) failed to abolish the neutrophil CA. After gel filtration the greater part of the neutrophil CA (80%) was recovered among low-molecular-weight components (300 to 1300 daltons). A preliminary deactivation of PMN by leukotriene B4 suppressed the CA of AM supernatants. These results indicate that IgE-dependent stimulation of AMs produces a neutrophil and eosinophil CA, present in a low-molecular-weight fraction possibly related to leukotrienes, and emphasizes the role of AMs in inflammatory lung processes during allergic asthma. 相似文献
7.
目的:探讨哮喘患者痰液嗜酸性粒细胞凋亡(EOS)与IL-5和sIL-2R的关系。方法:选择哮喘患者(哮喘组)急性发作期和缓解期30例,20名健康人(正常组)作对照。分别采用ELISA法测定患者痰液白细胞介素5(IL-5)和可溶性白介素2受体(sIL-2R),应用流式细胞仪检测痰液EOS凋亡。结果:哮喘患者急性发作期和缓解期痰液中IL-5和sIL-2R明显升高,EOS凋亡率增高,而正常组未发现EOS凋亡。急性发作期哮喘患者EOS凋亡率与IL-5呈明显的负相关,r为~0.78。结论:哮喘患者气道局部有EOS凋亡现象,并受到IL-5相互作用的调节。sIL-2R与EOS凋亡率无明显的相关性。 相似文献
8.
9.
Multiple molecular species of the eosinophil chemoattractant platelet activating factor (PAF) are produced as a result of inflammatory processes. We therefore compared the ability of three naturally occurring PAF species (C160, C180, and C181), which only varied at carbon 1, to induce eosinophil chemotaxis through naked 3-m pore polycarbonate filters. Timecourse experiments indicated that all species of PAF tested induced significant and equivalent eosinophil migration at 1 h which peaked at 2 h. Overall, the rank order of chemotactic potency for the PAF species was relatively equivalent. The specific PAF antagonist WEB 2086 inhibited eosinophil migration induced by all three PAF species equally. We conclude that the degree of PAF-induced eosinophil migration is not dependent upon the molecular species of PAF.accepted by G. W. CarterThis work was supported in part by a Veterans Administration Merit Review Award. 相似文献
10.
Allergic diseases are characterized by the presence of eosinophils, which are recruited to the affected tissues by chemoattractants produced by T cells, mast cells and epithelium. Our objective was to evaluate if allergens can directly activate human eosinophils. The capacity of purified allergen extracts to elicit eosinophil chemotaxis, respiratory burst, degranulation and up-regulation of the adhesion molecule complement receptor 3 (CR3) was determined in eosinophils isolated from healthy blood donors. Eosinophils stimulated with an extract from house dust mite (HDM) released the granule protein major basic protein (MBP) and up-regulated the surface expression of CR3. Cat allergen extracts also induced the up-regulation of CR3, but not the release of MBP; instead cat, as well as birch and grass allergens, elicited the release of eosinophil peroxidase (EPO). In addition, grass pollen extract caused the secretion of MBP. None of the allergens stimulated eosinophilic cationic protein release, nor production of free oxygen radicals. Both HDM and birch extracts were chemotactic for eosinophils. These findings establish that common aeroallergens can directly activate eosinophils in vitro. We propose that eosinophil activation in vivo is not exclusively mediated by cytokines and chemokines of the allergic inflammatory reaction, but could partly be the result of direct interaction between allergens and eosinophils. 相似文献