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ADP-ribosylation: role in LPS-induced phosphorylation of two cytosolic proteins (p36/38) in monocytes. adp核糖基化:在单核细胞中脂多糖诱导的两种胞质蛋白(p36/38)磷酸化中的作用。
S Hauschildt, A J Ulmer, H D Flad, T Heyden, H Heine

Human monocytes respond to LPS by releasing proinflammatory cytokines such as TNF-alpha, IL-1 and IL-6. Here we show that inhibitors of ADP-ribosylation namely nicotinamide and meta-iodobenzylguanidine prevent production of TNF-alpha and IL-6 at the protein and mRNA level. The inhibitors also influence the LPS-induced phosphorylation pattern of cytosolic proteins. They consistently lead to changes of the phosphorylation state of two proteins with an apparent molecular mass of 36 kDa and 38 kDa. The changes are both time and dose dependent. The data suggest that the conditions leading to altered phosphorylation of p36/38 may correlate with conditions initiating and regulating TNF-alpha and IL-6 production.

人单核细胞通过释放促炎细胞因子如tnf - α、IL-1和IL-6来响应LPS。在这里,我们发现adp核糖基化的抑制剂,即烟酰胺和间碘苄基胍,在蛋白质和mRNA水平上阻止tnf - α和IL-6的产生。抑制剂也影响lps诱导的胞质蛋白磷酸化模式。它们一致地导致两种表观分子质量分别为36 kDa和38 kDa的蛋白磷酸化状态的变化。这些变化与时间和剂量有关。这些数据表明,导致p36/38磷酸化改变的条件可能与启动和调节tnf - α和IL-6产生的条件相关。
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引用次数: 0
The pathogenic role of LBP in gram-negative sepsis and septic shock. LBP在革兰氏阴性脓毒症和感染性休克中的致病作用。
D Heumann, S Lengacher, D Le Roy, C V Jongeneel, M P Glauser
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引用次数: 0
Natural and synthetic polypeptides that recognize the conserved lipid a binding site of lipopolysaccharides. 天然的和合成的多肽,识别保守的脂质是脂多糖的结合位点。
M Porro, A Rustici, M Velucchi, D Agnello, P Villa, P Ghezzi
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引用次数: 0
Structure-function analysis of soluble and membrane-bound CD14. 可溶性和膜结合CD14的结构-功能分析。
T N Kirkland, S Viriyakosol
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引用次数: 0
Role of nitric oxide and reactive oxygen species in endotoxin shock. 一氧化氮和活性氧在内毒素休克中的作用。
T Yoshikawa, H Takano, M Kondo
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引用次数: 0
Cytokine regulation of inducible nitric oxide synthase in vascular smooth muscle cells. 血管平滑肌细胞诱导型一氧化氮合酶的细胞因子调控。
J Cohen, T J Evans, J Spink

NO is an important mediator in sepsis. It has been unequivocally established that it is the major determinant in the vasodilatation and consequent hypotension in experimental animals following the administration of LPS. It is cytotoxic, particularly in combination with superoxide anions, and exerts negative inotropic and chronotropic effects on the heart. The exact role that these functions play in sepsis, however, remain unclear. Similarly, its immunomodulatory and cerebral effects, although potentially important, remain of uncertain significance in sepsis. Regulation of such a pivotal molecule is clearly extremely important: the data described here show that not only is this regulation extremely complex, but it appears to vary in different cell types. The implication of this finding for future clinical work is clear. NO production is not all bad: in some circumstances, it may be desirable to differentially regulate iNOS activity such that production is restricted in some cell types but not in others. The work described here begins to offer the possibility of identifying new molecular targets which allow this kind of differential regulation.

一氧化氮是脓毒症的重要介质。已经明确地确定,它是实验动物在给药LPS后血管扩张和随之而来的低血压的主要决定因素。它具有细胞毒性,特别是与超氧阴离子结合时,对心脏产生负性肌力和变时作用。然而,这些功能在败血症中发挥的确切作用尚不清楚。同样,它的免疫调节和脑作用,虽然可能重要,但在败血症中的意义仍不确定。这种关键分子的调控显然是极其重要的:这里描述的数据表明,这种调控不仅极其复杂,而且似乎在不同的细胞类型中有所不同。这一发现对未来临床工作的意义是明确的。一氧化氮的产生并不全是坏事:在某些情况下,可能需要对一氧化氮的活性进行差异调节,这样在某些细胞类型中产生一氧化氮受到限制,而在其他细胞类型中则没有。这里描述的工作开始提供识别允许这种差异调节的新分子靶标的可能性。
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引用次数: 0
Molecular mechanisms responsible for endotoxin tolerance. 内毒素耐受的分子机制。
B Yoza, K LaRue, C McCall

Bacterial lipopolysaccharide endotoxin (LPS) is a potent activator of a number of inflammatory genes, including interleukin-1 (IL-1). IL-1 and other cytokines such as tumor necrosis factor alpha (TNF alpha) are essential mediators in inducing severe sepsis syndromes (SS). Major cellular targets of LPS are blood or tissue leukocytes, such as macrophages and neutrophils. These cells can respond and adapt to LPS, the latter phenomenon is known as LPS tolerance. In animals, LPS tolerance is a highly effective mechanism of protection against the lethal syndrome of severe sepsis. Two models are used to investigate the molecular basis of LPS tolerance. The first model employs blood leukocytes isolated from patients with SS. The second model employs the promonocytic cell line, THP-1 in vitro. In the SS model, LPS tolerance of involves repression at the level of IL-1 beta mRNA. Suppression of IL-1 beta mRNA is under the control of a labile repressor protein. In contrast to suppression of IL-1 beta, mRNA is under the control of a labile repressor protein. In contrast to suppression of IL-1 beta, there is increased expression of the Type 2 IL-1 receptor mRNA and protein in leukocytes from patients with SS. The THP-1 model of LPS tolerance also involves repression of LPS induction of IL-1 beta gene expression. The repression of THP-1 cell IL-1 beta expression is at the level of transcription, and like the SS model is under the control of a labile protein. LPS tolerance in both models is stimulus-specific. We further find that transcription factors such as NF kappa B and AP-1 may participate in regulating LPS tolerance.

细菌脂多糖内毒素(LPS)是许多炎症基因的有效激活剂,包括白细胞介素-1 (IL-1)。IL-1和其他细胞因子如肿瘤坏死因子α (TNF α)是诱导严重脓毒症综合征(SS)的重要介质。LPS的主要靶细胞是血液或组织中的白细胞,如巨噬细胞和中性粒细胞。这些细胞能够对LPS产生反应和适应,后一种现象被称为LPS耐受。在动物中,脂多糖耐受性是一种非常有效的机制,可以防止严重败血症的致命综合征。两个模型被用来研究脂多糖耐受性的分子基础。第一种模型采用分离自SS患者的血白细胞,第二种模型采用体外培养的原单核细胞THP-1。在SS模型中,LPS耐受涉及IL-1 β mRNA水平的抑制。IL-1 β mRNA的抑制受一种不稳定的抑制蛋白的控制。与IL-1 β的抑制相反,mRNA受一种不稳定的抑制蛋白的控制。与抑制IL-1 β相反,SS患者白细胞中2型IL-1受体mRNA和蛋白的表达增加。LPS耐受的THP-1模型也涉及抑制LPS诱导IL-1 β基因表达。对THP-1细胞IL-1 β表达的抑制是在转录水平,与SS模型一样是受一种不稳定蛋白的控制。两种模型的LPS耐受性都是刺激特异性的。我们进一步发现转录因子如NF κ B和AP-1可能参与调节LPS耐受。
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引用次数: 0
The role of scavenger receptors in LPS-induced macrophage activation. 清道夫受体在lps诱导的巨噬细胞活化中的作用。
T Kirikae, T Kodama, F Kirikae, H Suzuki, M Nakano
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引用次数: 0
The role of tyrosine kinases and map kinases in LPS-induced signaling. 酪氨酸激酶和map激酶在脂多糖诱导的信号传导中的作用。
A L DeFranco, M T Crowley, A Finn, J Hambleton, S L Weinstein
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引用次数: 0
Production of nontoxic lipid A by chemical modification and its antagonistic effect on LPS activity. 化学修饰制备无毒脂质A及其对LPS活性的拮抗作用。
K Tanamoto
{"title":"Production of nontoxic lipid A by chemical modification and its antagonistic effect on LPS activity.","authors":"K Tanamoto","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":20686,"journal":{"name":"Progress in clinical and biological research","volume":"397 ","pages":"269-80"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20497115","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
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Progress in clinical and biological research
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