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排序方式: 共有445条查询结果,搜索用时 15 毫秒
1.
Seishiro Hirano Takako Asami Naomi Kodama Kazuo T. Suzuki 《Archives of toxicology》1994,68(7):444-449
In a preceding study, we reported that the numbers of macrophages and polymorphonuclear leukocytes (PMN) were increased in
bronchoalveolar lavage fluid (BALF) following the intratracheal instillation of nickel sulfate (NiSO4) in rats. In the present study, BALF chemotactic activities for both macrophages and PMN were measured to investigate if
the increases of these inflammatory cells in BALF depend on increases in chemotactic activities in epithelial lining fluid
(ELF) of the lung. Both the number of PMN and the PMN chemotactic activity peaked at 2 days post-instillation and they were
significantly correlated. However, the PMN chemotactic activity was inversely correlated with concentration of leukotriene
B4 (LTB4), a well-known chemotaxin. Although PMN were not observed in control BALF, LTB4 concentration in the control ELF (ca. 5×10–7 M) was estimated to have a potential to attract PMN chemotactically through a membrane in in vitro migration assay. These
results suggest that the presence of LTB4 in ELF itself does not trigger transpulmonary PMN infiltration. The rat BALF were fractionated by high performance liquid
chromatography (HPLC), and PMN chemotactic activity of each fraction was measured. The elution profiles of PMN chemotactic
activity showed that there were at least two different chemotaxins in BALF obtained from the NiSO4-exposed rats. Macrophage chemotactic activity in BALF also peaked at 2 days post-instillation. However, the number of macrophages
was not significantly correlated with the chemotactic activity for macrophage in BALF. The HPLC study showed that the macrophage
chemotactic substance in the BALF obtained from NiSO4-exposed rats was different from complement fragment (C5a) and its MW was estimated to be 10 – 12 kD.
Received: 1 December 1993/Accepted: 16 March 1994 相似文献
2.
D. van Riessen M. R. Daha T. J. M. Smeets F. C. Breedveld 《Rheumatology international》1992,12(1):1-5
Summary It has been suggested that the reduced resistance of patients with rheumatoid arthritis (RA) to bacterial joint infections may be due in part to polymorphonuclear cell (PMN) function. To obtain further insight into the mechanis that contribute to the increased susceptiblity of RA patients to such infections we investigated the influence of different solid surfaces on the ingestion of various bacterial strains by PMN. Both in the presence and absence of serum, phagocytosis of bacteria by PMN was significantly lower on monolayers of synovial fibroblasts as compared to monolayers of endothelial cells and embryonic fibroblasts. It could be shown that the relative influence of the solid surfac on the results of the phagocytosis assay increased when decreasing concentrations of purified IgG were used. The results of this study sugpurified IgG were used. The results of this study suggested that the effect of synovial fibroblasts on PMB may lead to reduced clearance of bacteria from the joint. 相似文献
3.
创伤性休克后血浆黏附分子的变化及不同复苏液的影响 总被引:7,自引:0,他引:7
目的 探讨创伤性休克兔中性粒细胞黏附分子CD11b、血清可溶性细胞间黏附分子(sICAM ) 1的动态变化及不同复苏液的影响。方法 72只创伤性休克模型兔分为 6组 ,林格氏液组按失血量 2倍输入乳酸林格氏液 ,其他各组按 6ml/kg分别输入右旋糖酐 40、70 6代血浆、7.5 %氯化钠和 2 0 %白蛋白。分别采用流式细胞仪、酶联免疫吸附法检测CD11b、sICAM 1表达值。结果 各实验组休克 1hCD11b及sICAM 1表达增高 ,与对照组比较差异有显著性 (P <0 .0 5 ) ,并于12h达最高值 (林格氏液组 85 .6± 12 .1,60 9.3± 10 1.3 ;高渗盐组 77.5± 10 .3 ,5 18.5± 87.2 ;白蛋白组 78.2± 10 .7,5 2 2 .4± 88.3 ;P <0 .0 1)。高渗盐和白蛋白组 2 4、48hCD11b和sICAM 1分别为5 9 .2± 6.9,5 4.6± 5 .9;3 60 .1± 68.4,2 74.4± 40 .1;5 8.9± 6.4,5 5 .0± 5 .8;3 5 2 .6± 65 .3 ,2 70 .2±3 8.2 ,较林格氏液组 (72 .3± 10 .1,65 .8± 8.3 ;5 0 2 .6± 84.5 ,3 42 .4± 63 .1)降低 (P <0 .0 5 ) ;高渗盐和白蛋白组 (8.3 % )复苏 48h动物死亡率较林格氏液组 (4 1.7% )低 (P <0 .0 5 )。结论 创伤性休克时PMNCD11b和sICAM 1表达增加 ;采用 7.5 %氯化钠或 2 0 %白蛋白复苏时表达值及死亡率较乳酸林格氏液低。 相似文献
4.
Karsten Schrör Christoph Thiemermann Peter Ney 《Naunyn-Schmiedeberg's archives of pharmacology》1988,338(3):268-274
Summary This study investigates the action of intravenous PGE1 on myocardial reperfusion injury and the possible involvement of antineutrophil activities. Cats were subjected to 3 h of temporary ligation of the left anterior descending coronary artery, followed by 2 h of reperfusion. Animals were treated with PGE1 (5 g/kg x min) or vehicle (saline solution), starting 0.5 h after coronary artery occlusion. Vehicle-treated cats exhibited a significant loss of cardiac creatine phosphokinase specific activity at 5 h, accompanied by a significant ischemia-induced rise in the ST segment of the ECG and development of a Q wave after starting reperfusion. All of these alterations were largely prevented by PGE1 treatment. PGE1 exerted some blood-pressurelowering activity at 5 h (P > 0.05) but did not reduce myocardial contractile force and oxygen consumption. PGE1 modestly antagonized ischemia-induced formation of platelet aggregates. However, PGE1 prevented the rise in peripheral white blood cell count during ischemia and reperfusion and inhibited the generation of reactive oxygen species (myeloperoxidase assay) from zymosan-stimulated whole blood ex vivo. The ratio of generation of reactive oxygen species/white blood count remained unchanged. It is concluded that PGE1 protects the ischemic myocardium from acute reperfusion injury and that this effect involves an action of the compound on neutrophils, probably by improved myocardial tissue preservation, resulting in reduced formation of chemotactic products and, consequently, less local neutrophil accumulation and release of noxious metabolites.Parts of these results have been presented to the 29th Spring meeting of the Deutsche Gesellschaft für Pharmakologie und Toxikologie, Mainz, 1988
Send offprint requests to K. Schrör at the above address 相似文献
5.
Tadaaki Yokota Tokuhiro Ishihara Hiroo Kawano Mutsuo Takahashi Yoshimi Yamashita Toshikazu Gondo Yoshihiro Fujinaga Fumiya Uchino 《Pathology international》1989,39(6):349-355
Amyloid enhancing factor (AEF) was extracted from spleens of mice that had received amyloidogenic stimulation. Sephacryl S 300 gel filtration of the crude AEF yielded five fractions, among which strong AEF activity was present in the first peak (Fl), and confirmed by an amyloid induction experiment. An anti AEF antiserum was obtained from a rabbit by immunization with Fl. This antibody reacted strongly with splenic polymorphonuclear leukocytes (PML) from mice given amyloidogenic stimulation, and weakly with those from normal untreated mice. Isoelectric focusing (IEF) analysis of both Fl and sera from mice given amyloidogenic stimulation was performed. A single band was observed on IEF analysis of Fl, whereas many bands were seen on IEF analysis of the sera. After the substances in the gel had been transferred to nitrocellulose membranes by capillary blotting, the membranes were made to react with the anti-AEF antiserum. The results suggested that AEF is a high molecular-weight substance derived from PML and increases in the serum at the time of, or shortly prior to, amyloid deposition in the spleen. Acta Pathol Jpn 39: 349∼355, 1989. 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.
Malyak Mark Smith Michael F. Abel Ashley A. Arend William P. 《Journal of clinical immunology》1994,14(1):20-30
Journal of Clinical Immunology - The objective of this study was to characterize interleukin-1 receptor antagonist (IL-1ra) and interleukin-1β (IL-1β) production by human peripheral blood... 相似文献
8.
Objective: This study investigated the effects of insulin on the phagocytosis of C3bi – and IgG-opsonized yeast particles in normal
human neutrophils.
Methods: Neutrophils were incubated in different insulin concentrations for 30 minutes and stimulated by C3bi – or IgG-opsonized yeast
particles. Phagocytosis was quantified by both light microscopy and FACscan flow cytometry. Laser confocal microscopy was
used for quantification of F-actin levels.
Results: Elevated insulin concentrations decreased neutrophil phagocytosis of both types of targets. This defect was shown to be in
part due to a delayed phagocytosis in the presence of insulin. Following a 30 minute incubation, insulin was found to increase
the accumulation of cortical F-actin, without affecting the total cellular F-actin content. The specific PKCα/β inhibitor,
Go6976, abolished the insulin-mediated increase in cortical F-actin content and both Go6976 and the PKCα/β/δ/ε-specific inhibitor
GF109203X reversed the inhibitory effects of insulin on phagocytosis.
Conclusion: Hyperinsulinemia in vitro can inhibit phagocytosis of opsonized targets in normal human neutrophils. This effect of insulin is dependent on activation
of PKCα and/or PKCβ, and these insulin signals may interfere with the dynamic assembly/disassembly and/or distribution of
F-actin, which is required for the phagocytosis process.
Received 8 July 2005; accepted 13 October 2005 without revision I. Ahnfelt-R?nne 相似文献
9.
Transmission electron microscopy of thin sections of the rat incisor pulp revealed that in the middle region of the incisor there were fenestrated capillaries in the “predentinal plexus” and that this region contained the tallest odontoblasts. The odontoblasts gradually became shortened in the incisal part of this region: the fenestrated capillaries in the predentinal plexus changed to continuous type capillaries. Almost all the odontoblasts had degenerated near the incisal end of the tooth. The predentinal plexus disappeared in this region, but the “subodontoblastic capillary plexus” persisted. In a specific region just beneath the worn incisal end, numerous macrophages and polymorphonuclear neutrophils appeared and scavenged the degenerating cells, possibly including the odontoblasts. © 1993 Wiley-Liss, Inc. 相似文献
10.
Several age-related alterations occur at the cellular level in the immune system leading to a decrease in the immune response. The present study was designed to determine the effect of L-carnitine on impaired neutrophil functions of aged rats. For this reason, superoxide anion radical production, chemotaxis and phagocytic activity were studied in the neutrophils obtained from the peripheral blood of young and old rats. We orally gavaged L-carnitine (50 mg/kg b.w. per day) or control vehicle into young (2 months) and aged (24 months) rats for 30 consecutive days. The neutrophils of aged rats exhibited an increase in superoxide anion production and decline in phagocytosis and chemotaxis when compared with that in young rat neutrophils. Superoxide anion production in aged rats was significantly decreased by L-carnitine treatment which was accompanied with a significant enhancement of chemotactic and phagocytic activity being restored to control levels. These findings demonstrated that L-carnitine is capable of restoring the age-related changes of neutrophil functions. 相似文献