Journal of endotoxin research最新文献_第8页

Localization of the mouse defense lectin ficolin B in lysosomes of activated macrophages 小鼠防御凝集素ficolin B在活化巨噬细胞溶酶体中的定位

Journal of endotoxin research Pub Date : 2006-04-01 DOI: 10.1177/09680519060120020801

V. Runza, T. Hehlgans, B. Echtenacher, U. Zähringer, W. Schwaeble, D. Männel

引用次数: 34

Liver argininosuccinate synthase binds to bacterial lipopolysaccharides and lipid A and inactivates their biological activities 肝精氨酸琥珀酸合成酶与细菌脂多糖和脂质A结合并使其生物活性失活

Journal of endotoxin research Pub Date : 2006-02-01 DOI: 10.1177/09680519060120010301

M. Satoh, Tsuguya Iwahori, N. Sugawara, M. Yamazaki

{"title":"Liver argininosuccinate synthase binds to bacterial lipopolysaccharides and lipid A and inactivates their biological activities","authors":"M. Satoh, Tsuguya Iwahori, N. Sugawara, M. Yamazaki","doi":"10.1177/09680519060120010301","DOIUrl":"https://doi.org/10.1177/09680519060120010301","url":null,"abstract":"The liver is known to clear and detoxify circulating lipopolysaccharide (LPS). To characterize the molecules involved in this process in the liver, we attempted to purify mouse liver protein(s) that can interact with lipid A, a biologically active portion of LPS. By partially purifying the inactivating activity against a synthetic lipid A analog, we observed the enrichment of a 45-kDa protein in the active fractions. The internal amino acid sequences of the protein were identical with those of argininosuccinate synthase (EC 6.3.4.5). To examine whether argininosuccinate synthase can interact with lipid A, we purified the enzyme from mouse liver and found the co-elevation of the specific enzyme activity and specific lipid A-inactivating activity, indicating that argininosuccinate synthase is the major lipid A-interacting protein in liver. Argininosuccinate synthase also inhibited the biological activities (macrophage activation and Limulus test) of natural lipid A and rough-type LPS but not smooth-type LPS. The enzyme activity was inhibited by lipid A and rough-type LPS and also by smooth-type LPS. Native gel electrophoresis of a mixture of argininosuccinate synthase and LPS and immunoprecipitation of a mixture of argininosuccinate synthase and [3H]-LPS with anti-argininosuccinate synthase antiserum showed that argininosuccinate synthase stably bound lipid A and LPS. These findings, together, indicate that argininosuccinate synthase can effectively bind LPS in the liver.","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"12 1","pages":"21 - 38"},"PeriodicalIF":0.0,"publicationDate":"2006-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/09680519060120010301","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65208095","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: 16

GM-CSF priming of human monocytes is dependent on ERK1/2 activation 人单核细胞的GM-CSF的启动依赖于ERK1/2的激活

Journal of endotoxin research Pub Date : 2006-02-01 DOI: 10.1177/09680519060120010201

S. Lendemans, Meenakshi Rani, C. Selbach, E. Kreuzfelder, F. Schade, S. Flohe

{"title":"GM-CSF priming of human monocytes is dependent on ERK1/2 activation","authors":"S. Lendemans, Meenakshi Rani, C. Selbach, E. Kreuzfelder, F. Schade, S. Flohe","doi":"10.1177/09680519060120010201","DOIUrl":"https://doi.org/10.1177/09680519060120010201","url":null,"abstract":"The ability to augment monocyte functions such as TNF-α-producing capacities confers a high immunostimulating potential to GM-CSF. In the present investigation, the mechanism of the GM-CSF-mediated enhancement of monocyte cytokine production was analysed with regard to the involvement of intracellular signalling pathways. GM-CSF primes human monocytes dose- and time-dependently for enhanced LPS-stimulated TNF-α synthesis. Pre-incubation with 10 ng/ml GM-CSF for 6 h before LPS stimulation (10 ng/ml) caused a 3.4 ± 1.9-fold increase in TNF-α release compared to unprimed controls. This was associated with increased phosphorylation of IκBα and elevated nuclear levels of the NF-κB components p50 and p65 and NF-κB binding to DNA. LPS-induced AP-1 binding to DNA was also enhanced in GM-CSF-pre-incubated cells. GM-CSF treatment also caused a slight increase in TLR4 expression on monocytes while CD14 expression remained unchanged. GM-CSF-priming was unaffected by inhibitors of p38 MAPK (SB203580) and lipoxygenase (NDGA). In contrast, the broad-spectrum tyrosine kinase inhibitor genistein and the MEK-1 inhibitor (PD98059) abrogated GM-CSF priming of TNF-α release and activation of both NF-κB and AP-1. It is concluded that a tyrosine kinase of the GM-CSF-triggered ERK1/2 pathway augments the LPS-induced NF-κB and AP-1 activation.","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"12 1","pages":"10 - 20"},"PeriodicalIF":0.0,"publicationDate":"2006-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/09680519060120010201","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65208058","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: 20

Reduced toxicity of lipo-oligosaccharide from a phoP mutant of Neisseria meningitidis: an in vitro demonstration 降低来自脑膜炎奈瑟菌phoP突变体的脂寡糖的毒性:一项体外证明

Journal of endotoxin research Pub Date : 2006-02-01 DOI: 10.1177/09680519060120010401

T. Rustam, S. McClean, J. Newcombe, J. McFadden, L. Eales-Reynolds

{"title":"Reduced toxicity of lipo-oligosaccharide from a phoP mutant of Neisseria meningitidis: an in vitro demonstration","authors":"T. Rustam, S. McClean, J. Newcombe, J. McFadden, L. Eales-Reynolds","doi":"10.1177/09680519060120010401","DOIUrl":"https://doi.org/10.1177/09680519060120010401","url":null,"abstract":"PhoP is part of a two-component regulatory system, which we have previously demonstrated in Neisseria meningitidis and shown to be an important regulator of virulence in an in vivo model. The phoP mutant clearly induced cross-species reactive antibodies and lacks the obvious toxic effects of the wild-type strain. In the current study, we demonstrate distinct differences between the wild-type and mutant strains in an in vitro model of toxicity. At concentrations likely to be present early in an infection, the mutant was more efficient at stimulating an inflammatory response than the wild-type. However, at the concentrations likely to be found at the site of a fulminant infection, the mutant showed significantly weaker ability to stimulate the release of pro-inflammatory cytokines and the production of reactive oxygen and nitrogen intermediates. SDS-PAGE analysis of the isolated LOS from the wild-type and mutant showed a difference in the level of expression of two major species of LOS, a finding which was supported by preliminary MALDI-TOF analysis. These results suggest that the altered toxicity of the mutant may be due to the increased expression of a conformationally altered LOS species, which shows less affinity and avidity for the cellular receptors responsible for the inflammatory response to endotoxin.","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"2 1","pages":"39 - 46"},"PeriodicalIF":0.0,"publicationDate":"2006-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/09680519060120010401","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65208106","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: 7

Pro-atherogenic properties of lipopolysaccharide from the periodontal pathogen Actinobacillus actinomycetemcomitans 牙周病原体放线菌脂多糖的促动脉粥样硬化特性

Journal of endotoxin research Pub Date : 2006-02-01 DOI: 10.1177/09680519060120010601

L. Lakio, M. Lehto, Anita M. Tuomainen, M. Jauhiainen, E. Malle, S. Asikainen, P. Pussinen

{"title":"Pro-atherogenic properties of lipopolysaccharide from the periodontal pathogen Actinobacillus actinomycetemcomitans","authors":"L. Lakio, M. Lehto, Anita M. Tuomainen, M. Jauhiainen, E. Malle, S. Asikainen, P. Pussinen","doi":"10.1177/09680519060120010601","DOIUrl":"https://doi.org/10.1177/09680519060120010601","url":null,"abstract":"Periodontitis is a common bacterial infection that affects tooth-supporting tissues and may eventually lead to tooth loss. The number and proportion of Gram-negative bacteria are extensively elevated in the pathologically deepened inflamed periodontal pockets.1 Chronic infections (e.g. periodontitis) have been linked to an increased risk for atherosclerosis,2 a progressive disease characterized by the accumulation of lipids and fibrous elements in the large arteries. The mechanisms behind the association between periodontitis and atherosclerosis are largely unknown, but may include bacteria-derived activation of inflammatory reactions systemically and in the arterial wall, enhanced cytokine production, low-density lipoprotein (LDL) modifications, lipoprotein-derived cholesterol/cholesteryl ester (CE) enrichment of macrophages,3 and adverse alterations in the lipoprotein profile resulting in decreased levels of anti-atherogenic, high-density lipoprotein (HDL).4 Periodontitis further causes changes in the activities of HDL conversion factors, which is paralleled by alterations in HDL composition and subclass distribution leading to an","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"12 1","pages":"57 - 64"},"PeriodicalIF":0.0,"publicationDate":"2006-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/09680519060120010601","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65208150","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: 9

Apoptosis induction in gastric mucous cells in vitro: lesser potency of Helicobacter pylori than Escherichia coli lipopolysaccharide, but positive interaction with ibuprofen 体外诱导胃粘膜细胞凋亡:幽门螺杆菌的效力低于大肠杆菌脂多糖，但与布洛芬有正相互作用

Journal of endotoxin research Pub Date : 2006-02-01 DOI: 10.1177/09680519060120010501

Emma Durkin, A. Moran, P. J. Hanson

{"title":"Apoptosis induction in gastric mucous cells in vitro: lesser potency of Helicobacter pylori than Escherichia coli lipopolysaccharide, but positive interaction with ibuprofen","authors":"Emma Durkin, A. Moran, P. J. Hanson","doi":"10.1177/09680519060120010501","DOIUrl":"https://doi.org/10.1177/09680519060120010501","url":null,"abstract":"Non-steroidal anti-inflammatory drugs (NSAIDs) cause peptic ulcer disease, but whether they interact with Helicobacter pylori to promote damage is controversial. Moreover, the reported induction of apoptosis in gastric cells by H. pylori lipopolysaccharide (LPS) (10—9 g/ml) contrasts with studies showing low immunological potency of this LPS. Therefore, the effects of LPS from H. pylori NCTC 11637 and Escherichia coli O111:B4 on apoptosis in a primary culture of guinea-pig gastric mucous cells were investigated in the presence and absence of the NSAID, ibuprofen. Cell loss was estimated by a crystal violet assay, and apoptosis determined from caspase activity and from condensation and fragmentation of nuclei. Exposure to E. coli LPS for 24 h caused cell loss and enhanced apoptotic activity at concentrations ≥ 10—9 g/ml, but similar effects were only obtained with H. pylori LPS at concentrations ≥ 10— 6 g/ml. Although ibuprofen (250 µM) caused cell loss and apoptosis, addition of either E. coli or H. pylori LPSs further enhanced these effects. In conclusion, LPS and ibuprofen interact to enhance gastric cell loss and apoptosis. In such interactions, E. coli LPS is more potent than that of H. pylori. The low potency of H. pylori LPS may contribute to a chronic low-grade gastritis that can be enhanced by the use of NSAIDs.","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"12 1","pages":"47 - 56"},"PeriodicalIF":0.0,"publicationDate":"2006-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/09680519060120010501","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65208141","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: 21

Review: Structural features and structural variability of the lipopolysaccharide of Yersinia pestis, the cause of plague 综述:引起鼠疫的鼠疫耶尔森菌脂多糖的结构特征和结构变异性

Journal of endotoxin research Pub Date : 2006-02-01 DOI: 10.1177/09680519060120010101

Y. Knirel, S. V. Dentovskaya, S. Senchenkova, R. Z. Shaikhutdinova, N. A. Kocharova, Andrey P. Anisimov

引用次数: 40

The interferon response to bacterial and viral infections. 干扰素对细菌和病毒感染的反应。

Journal of endotoxin research Pub Date : 2006-01-01 DOI: 10.1179/096805106X118799

Eric M Pietras, Supriya K Saha, Genhong Cheng

{"title":"The interferon response to bacterial and viral infections.","authors":"Eric M Pietras, Supriya K Saha, Genhong Cheng","doi":"10.1179/096805106X118799","DOIUrl":"https://doi.org/10.1179/096805106X118799","url":null,"abstract":"Type I interferons (IFNs) were first described several decades ago as soluble factors that were capable of 'interfering' with viral replication when added to infected cells. Type I IFNs have been shown to be induced by recognition of viral DNA and RNA via three distinct pathways: (i) a TRIF-dependent pathway in macrophages via TLRs 3 and 4; (ii) a MyD88-dependent pathway in plasmacytoid dendritic cells (pDCs) via TLRs 7/8 and 9; and (iii) an intracellular recognition pathway utilizing the cytoplasmic receptors RIG-I/MDA5. Interestingly, these viral recognition pathways converge on TRAF3, which induces interferon through the activation of IRF3 or IRF7 by the TBK-1 and IKKi complexes. While type I IFN has been traditionally associated with antiviral responses, recent studies have demonstrated that many bacteria also induce type I interferon responses. The mechanisms of type I IFN induction and its role in host defense, however, are largely unclear. Studies with the Gram-positive intracellular bacterium Listeria monocytogenes indicated that it may trigger type I IFN induction through novel TLR-independent intracellular receptors and type I IFN may play a detrimental role to host response against listerial infection. In this article, we summarize some of these findings and discuss the functional differences of type I IFNs in bacterial and viral infections.","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"12 4","pages":"246-50"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1179/096805106X118799","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26295769","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

Inflammatory, coagulatory and circulatory responses to logarithmic increases in the endotoxin dose in the anaesthetised pig. 麻醉猪内毒素剂量呈对数增长时的炎症、凝血和循环反应。

Journal of endotoxin research Pub Date : 2006-01-01 DOI: 10.1179/096805106X89053

Miklós Lipcsey, Anders Larsson, Mats B Eriksson, Jan Sjölin

{"title":"Inflammatory, coagulatory and circulatory responses to logarithmic increases in the endotoxin dose in the anaesthetised pig.","authors":"Miklós Lipcsey, Anders Larsson, Mats B Eriksson, Jan Sjölin","doi":"10.1179/096805106X89053","DOIUrl":"https://doi.org/10.1179/096805106X89053","url":null,"abstract":"Although porcine intravenous endotoxin shock models are widely employed in experimental sepsis, endotoxin dose-effect studies are scarce. Our primary aim was to establish the dose response to increasing endotoxin doses in inflammatory, coagulatory and haemodynamic effect variables, as well as to determine the optimal time point for assessment in a pig model. A secondary aim was to study pathophysiological covariations between the different responses. Twenty anaesthetised piglets received endotoxin intravenously in doses of 0.063 (n = 3), 0.25 (n = 3), 1.0 (n = 3), 4.0 (n = 3), 8 (n = 3) and 16 microg/kg/h (n = 2). In addition, non-endotoxin piglets constituted a control group (n = 3). Physiological variables were registered and blood samples analysed for TNF-alpha, IL-6, leukocyte, platelet and haemoglobin concentrations hourly for 6 h. Increases in the endotoxin dose induced significant log-log cytokine responses as well as log-linear leukocyte and platelet responses. Significant log-linear responses were observed for circulatory parameters, plasma leakage, hypoperfusion and pulmonary compliance. Significant covariations in the responses were noted. In conclusion, there were log-log or log-linear responses to endotoxin suggesting a greater effect of a given dose at lower pre-existing endotoxin concentrations and lower doses of < or = 1 microg/kg/h may be of advantage in experiments designed to study potential anti-endotoxin effects of experimental drugs or measures.","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"12 2","pages":"99-112"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1179/096805106X89053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26014724","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

Tolerance to microbial TLR ligands: molecular mechanisms and relevance to disease. 对微生物TLR配体的耐受性：分子机制及其与疾病的相关性。

Journal of endotoxin research Pub Date : 2006-01-01 DOI: 10.1179/096805106X102255

Andrei E Medvedev, Ian Sabroe, Jeffrey D Hasday, Stefanie N Vogel

{"title":"Tolerance to microbial TLR ligands: molecular mechanisms and relevance to disease.","authors":"Andrei E Medvedev, Ian Sabroe, Jeffrey D Hasday, Stefanie N Vogel","doi":"10.1179/096805106X102255","DOIUrl":"10.1179/096805106X102255","url":null,"abstract":"Many host cell types, including endothelial and epithelial cells, neutrophils, monocytes, natural killer cells, dendritic cells and macrophages, initiate the first line of defense against infection by sensing conserved microbial structures through Toll-like receptors (TLRs). Recognition of microbial ligands by TLRs induces their oligomerization and triggers intracellular signaling pathways, leading to production of pro- and anti-inflammatory cytokines. Dysregulation of the fine molecular mechanisms that tightly control TLR signaling may lead to hyperactivation of host cells by microbial products and septic shock. A prior exposure to bacterial products such as lipopolysaccharide (LPS) may result in a transient state of refractoriness to subsequent challenge that has been referred to as 'tolerance'. Tolerance has been postulated as a protective mechanism limiting excessive inflammation and preventing septic shock. However, tolerance may compromise the host's ability to counteract subsequent bacterial challenge since many septic patients exhibit an increased incidence of recurrent bacterial infection and suppressed monocyte responsiveness to LPS, closely resembling the tolerant phenotype. Thus, by studying mechanisms of microbial tolerance, we may gain insights into how normal regulatory mechanisms are dysregulated, leading ultimately to microbial hypo-responsiveness and life-threatening disease. In this review, we present current theories of the molecular mechanisms that underlie induction and maintenance of 'microbial tolerance', and discuss the possible relevance of tolerance to several infectious and non-infectious diseases.","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"12 3","pages":"133-50"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26041354","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