Journal of inflammation最新文献_第6页

Reactivity of murine and human recombinant LPS-binding protein (LBP) within LPS and gram negative bacteria. 鼠和人重组LPS结合蛋白(LBP)在LPS和革兰氏阴性菌中的反应性。

Journal of inflammation Pub Date : 1995-01-01

S Lengacher, C V Jongeneel, D Le Roy, J D Lee, V Kravchenko, R J Ulevitch, M P Glauser, D Heumann

引用次数: 0

Evidence for an intracellular activation loop in the IL-1 system. IL-1系统中存在细胞内激活环的证据。

Journal of inflammation Pub Date : 1995-01-01

R Hofmeister, D N Männel, W Falk

引用次数: 0

Molecular mechanism in tolerance to lipopolysaccharide. 脂多糖耐受性的分子机制。

Journal of inflammation Pub Date : 1995-01-01

H W Ziegler-Heitbrock

{"title":"Molecular mechanism in tolerance to lipopolysaccharide.","authors":"H W Ziegler-Heitbrock","doi":"","DOIUrl":"","url":null,"abstract":"Stimulation with lipopolysaccharide (LPS) will lead to the expression of a variety of genes in CD14+ monocytes/macrophages, but also in CD14- fibroblasts and endothelial cells. Upon secondary LPS stimulation, the expression of many of these genes is only minimal. This applies to several cytokines, most prominent among them tumor necrosis factor (TNF). Induction of tolerance appears to require some degree of activation in the primary exposure, as partial structures of LPS induce tolerance, as long as they are able to activate cells. Studies on the mechanism of unresponsiveness in tolerant cells show that the CD14 LPS receptor is not downregulated but may even increase in number at the cell surface. Furthermore, this receptor appears to be functional in that mobilization of the transcription factor NF-kappa B does still occur. This NF-kappa B complex is composed primarily of p50p50 homodimers, that bind to the respective DNA motif in the promoter region of many proinflammatory genes, thereby blocking transactivation. However, LPS tolerance does not lead to downregulation of all kinds of response, as some genes are even increased in expression upon secondary stimulation; these include p50 of NF-kappa B, TNF receptor type II and interleukin-10 (IL-10). These gene products are involved in the downregulation of proinflammatory cytokines and may thereby be instrumental in the unresponsiveness observed. Hence, tolerance to LPS is not a passive process that occurs in an exhausted cell; rather, it is a well-controlled active response that is orchestrated in order to prevent excessive inflammation. Important modulators of tolerance are glucocorticoids, which result in a general decrease of gene expression, and interferon-gamma (IFN-gamma), which enhances expression of proinflammatory genes. LPS tolerance does occur in some clinical settings, as in hemodialysis, in sepsis and in patients treated repeatedly with LPS or other monocyte activators. In fact, LPS tolerance may be exploited for prophylaxis of severe sepsis in patients at risk.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"45 1","pages":"13-26"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18588856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tumor necrosis factor (TNF)-induced cutaneous necrosis is mediated by TNF receptor 1. 肿瘤坏死因子(TNF)诱导的皮肤坏死是由TNF受体1介导的。

Journal of inflammation Pub Date : 1995-01-01

S Amar, T E Van Dyke, H P Eugster, N Schultze, P Koebel, H Bluethmann

{"title":"Tumor necrosis factor (TNF)-induced cutaneous necrosis is mediated by TNF receptor 1.","authors":"S Amar, T E Van Dyke, H P Eugster, N Schultze, P Koebel, H Bluethmann","doi":"","DOIUrl":"","url":null,"abstract":"Tumor necrosis factor (TNF) is a central mediator of immune and inflammatory responses. Its activities have been shown to be mediated by two distinct receptors, TNFR1 (p55) and TNFR2 (p75). The cytoplasmic domains of both TNF receptors are unrelated, suggesting that they link to different intracellular signaling pathways. To determine their role in vivo in lipopolysaccharide (LPS)- and TNF-induced skin inflammatory necrosis, TNFR1-, TNFR2-, and TNF lymphotoxin-alpha (LT alpha)-deficient mice were used. Skin abscesses were experimentally induced with local application of TNF or LPS. Large macroscopic ulcerations were observed in TNF-injected wild-type animals and to a slightly lesser extent in TNFR2-deficient mice with tissue destruction in both cases extending deep into the dermis. Tissue destruction was accompanied by an intense immune infiltrate composed mainly of neutrophils, lymphocytes, and macrophages. TNFR1-deficient and TNFR1/TNFR2-double-deficient mice, however, did not exhibit any ulceration and showed only a very mild inflammatory infiltrate. In TNF/LT alpha-double ligand0-deficient animals, a moderate epidermal necrosis was observed with a reduced inflammatory infiltrate compared to wild-type animals. As with TNF injections, subcutaneous injection of LPS induced a comparable pattern of skin necrosis in wild-type and TNF receptor mutant mice, yet a slightly more acute inflammatory level was observed regardless of the type of animal tested. As found for TNF-induced skin necrosis, the extent of LPS-induced skin necrosis was reduced in TNF/LT alpha-deficient mice compared to wild-type animals. The present data strongly suggest that TNFR1, rather than TNFR2, is engaged in LPS- and TNF-induced skin necrosis and highlight the predominant role played by TNF in LPS-induced inflammatory diseases.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"47 4","pages":"180-9"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20091951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Expression of nitric oxide synthase in human peripheral blood mononuclear cells and neutrophils. 一氧化氮合酶在人外周血单核细胞和中性粒细胞中的表达。

Journal of inflammation Pub Date : 1995-01-01

A R Amin, M Attur, P Vyas, J Leszczynska-Piziak, D Levartovsky, J Rediske, R M Clancy, K A Vora, S B Abramson

{"title":"Expression of nitric oxide synthase in human peripheral blood mononuclear cells and neutrophils.","authors":"A R Amin, M Attur, P Vyas, J Leszczynska-Piziak, D Levartovsky, J Rediske, R M Clancy, K A Vora, S B Abramson","doi":"","DOIUrl":"","url":null,"abstract":"It has been clearly demonstrated in rodents that nitric oxide (NO) plays an important role in host defense and immunity. However, evidence that human leukocytes express inducible nitric oxide synthase (iNOS) or its products has been inconclusive and a source of controversy. We report that iNOS could not be detected in human monocytes, HL-60 cells, neutrophils, and T cells by Western blotting analysis (< or = 10 pg) or by radiolabeled L-arginine-to-L-citrulline conversion (< or = 20 pmol L-citrulline) under conditions sufficient to induce iNOS in the rodent system and in human hepatocytes, which include activation with cytokines, endotoxins, and/or chemoattractants. However, sensitive methods such as RT-PCR and Northern blot analysis show \"constitutively expressed\" iNOS mRNA from human monocytes, neutrophils, Jurkat cells, and HL-60 cells. This iNOS mRNA is 4.4 kb and is similar to that seen in human hepatocytes and rodent macrophages. In spite of the constitutive expression of mRNA in neutrophils and the lack of detectable NOS activity (based on Western blotting and L-arginine-to-L-citrulline conversion assay), stimulation of human neutrophils unit FMLP in vitro induced the ADP-ribosylation of an intracellular NO target, glyceraldehyde-3-PO4 dehydrogenase (GAPDH), in a NO-dependent manner. These studies indicate that low levels of NOS protein are expressed in neutrophils (and perhaps T cells and monocytes) and produce NO following stimulation. The data indicate that, in addition to its phagocytic and tumoricidal activity. NO may also function as an autacoid signaling molecule within the cells.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"47 4","pages":"190-205"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20091989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Plasma interleukin 8 and polymorphonuclear leukocyte elastase concentrations in patients with septic shock. 脓毒性休克患者血浆白细胞介素8和多形核白细胞弹性酶浓度。

Journal of inflammation Pub Date : 1995-01-01

S Endo, K Inada, M Ceska, T Takakuwa, Y Yamada, H Nakae, T Kasai, H Yamashita, K Taki, M Yoshida

{"title":"Plasma interleukin 8 and polymorphonuclear leukocyte elastase concentrations in patients with septic shock.","authors":"S Endo, K Inada, M Ceska, T Takakuwa, Y Yamada, H Nakae, T Kasai, H Yamashita, K Taki, M Yoshida","doi":"","DOIUrl":"","url":null,"abstract":"We determined the plasma concentrations of interleukin 8 (IL-8), polymorphonuclear leukocyte elastase (PMNE), and endotoxin in patients with septic shock in order to investigate the role of IL-8 and PMNE in the development of septic shock, especially in septic adult respiratory distress syndrome (ARDS). The IL-8 concentration in patients with septic shock was 6.28 +/- 9.00 ng/mL (mean +/- SD, n = 29), which was significantly higher (P < 0.0001) than the concentration in septic patients without shock (0.35 +/- 0.35 ng/mL, n = 40). There was a significant correlation between the IL-8 concentration and the PMNE concentration at the onset of septic shock (r = 0.6916, P < 0.0001). The IL-8 concentration was also significantly correlated with the endotoxin concentration (r = 0.5584, P = 0.0016). There was a significant negative correlation (r = -0.8237, P < 0.0001) between the serum PMNE concentration and the oxygenation index (PaO2/FiO2) at the onset of septic shock. These results indicate that IL-8 and PMNE are produced in large quantities when septic shock occurs, and may play a role in the development of septic ARDS.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"45 2","pages":"136-42"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18588802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genetic dissection of inflammatory responses. 炎症反应的基因解剖。

Journal of inflammation Pub Date : 1995-01-01

J H Nadeau, L D Arbuckle, E Skamene

引用次数: 0

Tumor necrosis factor-alpha and interleukin-1 beta mediate human endothelial cell activation in blood at low endotoxin concentrations. 肿瘤坏死因子- α和白细胞介素-1 β在低内毒素浓度下介导血液中人内皮细胞的活化。

Journal of inflammation Pub Date : 1995-01-01

J Pugin, R J Ulevitch, P S Tobias

{"title":"Tumor necrosis factor-alpha and interleukin-1 beta mediate human endothelial cell activation in blood at low endotoxin concentrations.","authors":"J Pugin, R J Ulevitch, P S Tobias","doi":"","DOIUrl":"","url":null,"abstract":"Activation of endothelial cells by endotoxin (lipopolysaccharide, LPS) may occur through two different pathways. LPS can directly activate endothelial cells through its interaction with soluble CD14 or indirectly via cytokines produced in blood in response to LPS. Substitution of whole blood for plasma apparently increases the endothelial cells responses to LPS by a factor of 1,000, rendering them sensitive to subpicomolar quantities of LPS. This shift in sensitivity is dependent on the presence of monocytes or conditioned plasma from whole blood incubated with small concentrations of LPS. Herein, using agents that block the effects of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta), we demonstrate that TNF-alpha and IL-1 beta are the two LPS-induced cytokines responsible for the activation of endothelial cells, produced in blood in response to picomolar quantities of LPS. Anti-TNF-alpha monoclonal antibodies (mAbs) and IL-1 receptor antagonist separately had partial inhibitory effects. Complete and sustained inhibition of endothelial cell activation was obtained only when the two inhibitors were added together. We conclude that TNF-alpha and IL-1 beta induced in whole blood by picomolar concentrations of LPS mediate endothelial cell activation to these small quantities of LPS and that blocking of both cytokines is necessary to inhibit LPS-induced blood-dependent endothelial cell activation.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"45 1","pages":"49-55"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18588858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Regulation of GRO alpha production in human granulocytes. 人粒细胞GRO α生成的调控。

Journal of inflammation Pub Date : 1995-01-01

S Gasperini, F Calzetti, M P Russo, M De Gironcoli, M A Cassatella

{"title":"Regulation of GRO alpha production in human granulocytes.","authors":"S Gasperini, F Calzetti, M P Russo, M De Gironcoli, M A Cassatella","doi":"","DOIUrl":"","url":null,"abstract":"GRO alpha, a member of the chemokine superfamily, exerts potent stimulatory actions on granulocytes. In this report, we show that activated human polymorphonuclear leukocytes (PMN) are able to produce significant amounts of GRO alpha. Lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF alpha), and yeast particles opsonized with IgG (Y-IgG) had the ability to induce GRO alpha release, with Y-IgG being the most potent stimulus. The extracellular production of GRO alpha was also modulated by both interferon-gamma (IFN gamma) and interleukin-10 (IL-10). IFN gamma significantly inhibited the production of GRO alpha by PMN stimulated for 2 hr with LPS, TNF alpha, or Y-IgG, but potentiated the production of GRO alpha in cells stimulated for 18 hr with LPS and TNF alpha. IL-10 moderately suppressed the Y-IgG-induced production of GRO alpha, but strongly inhibited the action of LPS and potentiated the effect of TNF alpha. As revealed by Northern blot analysis, the extracellular production of GRO alpha under the experimental conditions used did not always correlate with parallel changes at the level GRO alpha mRNA expression, suggesting that production of GRO alpha by PMN might be regulated at post-transcriptional, translational, or post-translational level. These findings identify a novel biological function of PMN, likely involved in the modulation of the acute inflammatory response.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"45 3","pages":"143-51"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19577692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transgenic and knockout analyses of the role of TNF in immune regulation and disease pathogenesis. TNF在免疫调节和疾病发病机制中的作用的转基因和敲除分析。

Journal of inflammation Pub Date : 1995-01-01

E Douni, K Akassoglou, L Alexopoulou, S Georgopoulos, S Haralambous, S Hill, G Kassiotis, D Kontoyiannis, M Pasparakis, D Plows, L Probert, G Kollias

引用次数: 0