Journal of endotoxin research最新文献_第3页

Endotoxin-activated cultured neonatal rat cardiomyocytes express functional surface-associated interleukin-1alpha. 内毒素激活培养新生大鼠心肌细胞表达功能性表面相关白细胞介素-1 α。

Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907078609

Elena Westphal, Li Chen, Claudia Pilowski, Susanne Koch, Henning Ebelt, Ursula Müller-Werdan, Karl Werdan, Harald Loppnow

{"title":"Endotoxin-activated cultured neonatal rat cardiomyocytes express functional surface-associated interleukin-1alpha.","authors":"Elena Westphal, Li Chen, Claudia Pilowski, Susanne Koch, Henning Ebelt, Ursula Müller-Werdan, Karl Werdan, Harald Loppnow","doi":"10.1177/0968051907078609","DOIUrl":"https://doi.org/10.1177/0968051907078609","url":null,"abstract":"Interleukin-1 (IL-1) is a potent regulator of cardiovascular proliferation, apoptosis, contraction or production of inflammatory mediators. Thus, we investigated expression and function of IL-1 in cultured neonatal rat heart cells upon endotoxin stimulation. We show that cultured neonatal rat cardiomyocytes expressed IL-1alpha and IL-1beta mRNA. The cells expressed functional cell-associated IL-1 activity and a specific anti-IL-1alpha-antibody inhibited the activity. Biologically active IL-1alpha was present at the cell surface of the cardiomyocytes, as indicated in co-culture experiments. Immunohistochemistry showed IL-1alpha-staining of the neonatal cardiomyocytes. Although the cells also expressed IL-1beta mRNA, we did not detect IL-1beta in the supernatants of cultured cardiomyocytes by ELISA or in immunohistochemical staining. Furthermore, neonatal and adult rat heart tissues expressed IL-1alpha mRNA, whereas fetal, but not adult, human cardiac tissues expressed detectable IL-1alpha mRNA. In contrast, IL-1beta mRNA was present in rat and human fetal and adult samples. Furthermore, in patients with dilated or ischemic cardiomyopathy, we measured IL-1beta, but not IL-1alpha, mRNA. These results provide evidence for the presence of functionally active IL-1alpha on the cell surface of neonatal rat cardiomyocytes and may suggest a differential role of IL-1alpha in regulation of cellular functions during development, aging and disease in rat and human heart cells.","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 1","pages":"25-34"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907078609","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26822620","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: 10

High glucose up-regulates lipopolysaccharide-stimulated inflammatory cytokine production via c-jun N-terminal kinase in the monocytic cell line THP-1. 在单核细胞系THP-1中，高糖通过c-jun n -末端激酶上调脂多糖刺激的炎症细胞因子的产生。

Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907082608

Hirotaka Iwata, Yoshihiko Soga, Michio Meguro, Sayuri Yoshizawa, Yuka Okada, Yoshihiro Iwamoto, Akiko Yamashita, Shogo Takashiba, Fusanori Nishimura

{"title":"High glucose up-regulates lipopolysaccharide-stimulated inflammatory cytokine production via c-jun N-terminal kinase in the monocytic cell line THP-1.","authors":"Hirotaka Iwata, Yoshihiko Soga, Michio Meguro, Sayuri Yoshizawa, Yuka Okada, Yoshihiro Iwamoto, Akiko Yamashita, Shogo Takashiba, Fusanori Nishimura","doi":"10.1177/0968051907082608","DOIUrl":"https://doi.org/10.1177/0968051907082608","url":null,"abstract":"Diabetic subjects are susceptible to atherosclerosis. It has been postulated that inflammation plays a crucial role in atherogenesis. Since previous studies suggested persistent low-grade infection by Gram-negative bacteria such as Chlamydia spp. and/or periodontal infection is associated with increased atherogenesis among diabetic subjects, we hypothesized that macrophages under hyperglycemia respond to lipopolysaccharide (LPS) challenge in a more exaggerated manner than under normal glucose conditions. Therefore, we examined cytokine productivity and associated signal transduction molecules in LPS-stimulated the monocytic cell line THP-1, under conditions of hyperglycemia. Differentiated THP-1 cells were cultured under normal and high glucose conditions without fetal bovine serum, and were stimulated with Escherichia coli LPS in the presence of LPS binding protein. Following stimulation, activated signal transduction molecules were detected by protein microarray and confirmed thereafter. Results indicated that c-jun N-terminal kinase (JNK) was highly-phosphorylated at high glucose concentrations, and this was confirmed by Western-immunoblotting. Tumor necrosis factor-alpha and monocyte chemo-attractant protein-1 production were significantly enhanced under these conditions. SP600125, a selective inhibitor of JNK, dose-dependently suppressed the production of these cytokine. Therefore, we suggest that this may be one of the mechanisms by which sub-clinical infection by Gram-negative bacteria promotes atherosclerosis in diabetic subjects.","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 4","pages":"227-34"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907082608","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27065274","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: 22

The equine TLR4/MD-2 complex mediates recognition of lipopolysaccharide from Rhodobacter sphaeroides as an agonist. 马的TLR4/MD-2复合物作为激动剂介导对球形红杆菌脂多糖的识别。

Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907083193

Katharina L Lohmann, Michel L Vandenplas, Michelle H Barton, Clare E Bryant, James N Moore

{"title":"The equine TLR4/MD-2 complex mediates recognition of lipopolysaccharide from Rhodobacter sphaeroides as an agonist.","authors":"Katharina L Lohmann, Michel L Vandenplas, Michelle H Barton, Clare E Bryant, James N Moore","doi":"10.1177/0968051907083193","DOIUrl":"https://doi.org/10.1177/0968051907083193","url":null,"abstract":"Lipopolysaccharide (LPS) antagonists inhibit the response of inflammatory cells to LPS, presumably by competitive inhibition, and may be of therapeutic value in the treatment of endotoxemia and sepsis. The inhibitory effects of some LPS antagonists are restricted to certain host species, however, as the same molecules can have significant endotoxic activity in other species. This species-specific recognition appears to be mediated by Toll-like receptor 4 (TLR4) and/or MD-2. We have shown previously that LPS from Rhodobacter sphaeroides ( RsLPS) is an LPS antagonist in human cells but an agonist (or LPS mimetic) in equine cells. In the present study, HEK293 cells were transfected with combinations of human and equine CD14, TLR4 and MD-2, and incubated with either RsLPS or with LPS from Escherichia coli as an endotoxin control. NF-kappaB activation was measured in a dual luciferase assay as an indicator of cellular activation. Our results indicate that E. colic LPS activated NF-kappaB in cells transfected with all combinations of the three receptor proteins, whereas RsLPS activated NF-kappaB only in cells expressing the single combination of equine TLR4 and equine MD-2. We conclude that the TLR4/MD-2 complex is responsible for recognition of RsLPS as an agonist in equine cells.","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 4","pages":"235-42"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907083193","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27065275","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: 49

Lipopolysaccharide enhances interferon-gamma-induced nitric oxide (NO) production in murine vascular endothelial cells via augmentation of interferon regulatory factor-1 activation. 脂多糖通过增强干扰素调节因子-1的激活，增强干扰素γ诱导的小鼠血管内皮细胞一氧化氮(NO)的产生。

Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907080894

Naoki Koide, Mya Mya Mu, Ferdaus Hassan, Shamima Islam, Gantsetseg Tumurkhuu, Jargalsaikhan Dagvadorj, Yoshikazu Naiki, Isamu Mori, Tomoaki Yoshida, Takashi Yokochi

{"title":"Lipopolysaccharide enhances interferon-gamma-induced nitric oxide (NO) production in murine vascular endothelial cells via augmentation of interferon regulatory factor-1 activation.","authors":"Naoki Koide, Mya Mya Mu, Ferdaus Hassan, Shamima Islam, Gantsetseg Tumurkhuu, Jargalsaikhan Dagvadorj, Yoshikazu Naiki, Isamu Mori, Tomoaki Yoshida, Takashi Yokochi","doi":"10.1177/0968051907080894","DOIUrl":"https://doi.org/10.1177/0968051907080894","url":null,"abstract":"Lipopolysaccharide (LPS) enhances the production of nitric oxide (NO) in interferon (IFN)-gamma-stimulated vascular endothelial cells. We studied the mechanism by which LPS enhances IFN-gamma-induced NO production by using the murine vascular endothelial cell line, END-D. LPS enhanced IFN-gamma-induced NO production via augmented expression of inducible type NO synthase (iNOS) mRNA. LPS significantly augmented the activation of interferon regulatory factor (IRF)-1 in IFN-gamma-stimulated END-D cells, although it did not affect the activation of either MyD88-dependent nuclear factor (NF)-kappaB or MyD88-independent IRF-3. SB203580, an inhibitor of p38 mitogen-activated protein kinase (MAPK), prevented the nuclear translocation of IRF-1 in LPS and IFN-gamma-stimulated END-D cells, and inhibited the iNOS expression and NO production in those cells. Therefore, it is proposed that LPS enhanced NO production in IFN-gamma-stimulated END-D cells via augmenting p38 MAPKmediated IRF-1 activation.","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 3","pages":"167-75"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907080894","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26822451","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: 23

Chemical synthesis of peptidoglycan fragments for elucidation of the immunostimulating mechanism. 化学合成肽聚糖片段以阐明免疫刺激机制。

Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907080739

Yukari Fujimoto, Seiichi Inamura, Akiko Kawasaki, Zenyu Shiokawa, Atsushi Shimoyama, Takashi Hashimoto, Shoichi Kusumoto, Koichi Fukase

引用次数: 13

Priming, induction and modulation of plant defence responses by bacterial lipopolysaccharides. 细菌脂多糖对植物防御反应的启动、诱导和调节。

Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907079399

Mari-Anne Newman, J Maxwell Dow, Antonio Molinaro, Michelangelo Parrilli

{"title":"Priming, induction and modulation of plant defence responses by bacterial lipopolysaccharides.","authors":"Mari-Anne Newman, J Maxwell Dow, Antonio Molinaro, Michelangelo Parrilli","doi":"10.1177/0968051907079399","DOIUrl":"https://doi.org/10.1177/0968051907079399","url":null,"abstract":"Bacterial lipopolysaccharides (LPSs) have multiple roles in plant-microbe interactions. LPS contributes to the low permeability of the outer membrane, which acts as a barrier to protect bacteria from plant-derived antimicrobial substances. Conversely, perception of LPS by plant cells can lead to the triggering of defence responses or to the priming of the plant to respond more rapidly and/or to a greater degree to subsequent pathogen challenge. LPS from symbiotic bacteria can have quite different effects on plants to those of pathogens. Some details are emerging of the structures within LPS that are responsible for induction of these different plant responses. The lipid A moiety is not solely responsible for all of the effects of LPS in plants; core oligosaccharide and O-antigen components can elicit specific responses. Here, we review the effects of LPS in induction of defence-related responses in plants, the structures within LPS responsible for eliciting these effects and discuss the possible nature of the (as yet unidentified) LPS receptors in plants.","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 2","pages":"69-84"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907079399","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26822625","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: 151

Down-regulation of TGFbeta1 and leptin ameliorates thioacetamide-induced liver injury in lipopolysaccharide-primed rats. 下调TGFbeta1和瘦素可改善硫代乙酰胺诱导的大鼠肝损伤。

Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907081102

Huan-Nan Chen, Sabrina Fan, Ching-Feng Weng

{"title":"Down-regulation of TGFbeta1 and leptin ameliorates thioacetamide-induced liver injury in lipopolysaccharide-primed rats.","authors":"Huan-Nan Chen, Sabrina Fan, Ching-Feng Weng","doi":"10.1177/0968051907081102","DOIUrl":"https://doi.org/10.1177/0968051907081102","url":null,"abstract":"Pretreatment with a low dose of bacterial endotoxin (lipopolysaccharide, LPS) caused the reduction of cytochrome P450 (CYP) enzymes and inflammatory factors which are capable of protecting the liver from a lethal LPS challenge. However, the effects of LPS pretreatment on the expression of transforming growth factor beta1 (TGFbeta1) and leptin in thioacetamide (TAA)-induced liver fibrosis remain unknown. In this study, Sprague-Dawley rats were pretreated intraperitoneally with LPS (5 mg/kg body weight) for 24 h, and subsequently treated with TAA (200 mg/kg body weight/ 3 days) for 1 month to examine the effects of LPS on TAA-injured rats. LPS pretreatment was associated with lower granulation and lower (P < 0.05) GOT/GPT than in TAA-injured rats. The LPS-pretreated group had less collagen (Sirius red histochemical staining). Semiquantitative RT-PCR showed that the levels of collagen 3 and TGFbeta1 mRNAs were lower (P < 0.05) in the liver of LPS-pretreated rats than in TAA-injured rats. TGFbetaRI mRNA in the liver of LPS-pretreated rats exceeded (P < 0.05) that in TAA-injured rats. LPS pretreatment reduced the leptin content (Western blot) below that of TAA-injured rats. These results imply that LPS pretreatment (endotoxin tolerance) alleviates the TAA-induced liver fibrosis of rats by reducing TGFbeta1 and leptin content.","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 3","pages":"176-88"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907081102","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26822452","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

A tribute to Ernst Th. Rietschel: the gentleman scientist. 向恩斯特致敬。里切尔:绅士科学家。

Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907078603

Jean-Marc Cavaillon, Robert S Munford

引用次数: 0

Effects of human apolipoprotein A-I on endotoxin-induced leukocyte adhesion on endothelial cells in vivo and on the growth of Escherichia coli in vitro. 人载脂蛋白A-I对内毒素诱导的白细胞粘附内皮细胞和体外大肠杆菌生长的影响。

Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907078611

Premtip Thaveeratitham, Wanee Plengpanich, Worakamol Naen-Udorn, Suthiluk Patumraj, Weerapan Khovidhunkit

{"title":"Effects of human apolipoprotein A-I on endotoxin-induced leukocyte adhesion on endothelial cells in vivo and on the growth of Escherichia coli in vitro.","authors":"Premtip Thaveeratitham, Wanee Plengpanich, Worakamol Naen-Udorn, Suthiluk Patumraj, Weerapan Khovidhunkit","doi":"10.1177/0968051907078611","DOIUrl":"https://doi.org/10.1177/0968051907078611","url":null,"abstract":"Background: High-density lipoprotein (HDL) has been shown to inhibit leukocyte adhesion to endothelial cells induced by endotoxin in vivo and suppress the growth of bacteria in vitro; however, the components responsible for these effects, either lipids or proteins, are not yet defined. In this study, we examined the effects of apolipoprotein (apo) A-I, the major protein of HDL, on ameliorating the effect of endotoxin and inhibiting the growth of bacteria.Materials and methods: Apo A-I, purified from normal human HDL, was incubated with endotoxin. Leukocyte adhesion to endothelial cells of rat mesenteric venules was assessed using intravital fluorescence microscopy. Ability of apo A-I to inhibit the growth of Escherichia coli was assessed using a spread plate method.Results: Purified, lipid-free apo A-I could inhibit endotoxin-induced leukocyte adhesion to endothelial cells in vivo in a dose-dependent manner. In addition, apoA-I was able to suppress the growth of Escherichia coli in vitro.Conclusions: These data suggest that apo A-I of HDL can directly interact with endotoxin, ameliorating its effect and that apo A-I may have a direct toxic effect on whole bacteria. Therefore, therapeutic use of apo A-I in septicemia and bacterial infection should be further explored.","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 1","pages":"58-64"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907078611","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26822624","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: 19

Hemodynamic effects of titrated norepinephrine in healthy versus endotoxemic sheep. 去甲肾上腺素在健康绵羊和内毒素中毒绵羊体内的血流动力学影响。

Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907078614

Matthias Lange, Katrin Bröking, Christoph Hucklenbruch, Christian Ertmer, Hugo Van Aken, Martin Lücke, Hans-Georg Bone, Martin Westphal

{"title":"Hemodynamic effects of titrated norepinephrine in healthy versus endotoxemic sheep.","authors":"Matthias Lange, Katrin Bröking, Christoph Hucklenbruch, Christian Ertmer, Hugo Van Aken, Martin Lücke, Hans-Georg Bone, Martin Westphal","doi":"10.1177/0968051907078614","DOIUrl":"https://doi.org/10.1177/0968051907078614","url":null,"abstract":"In patients with sepsis and systemic inflammatory response syndrome, hemodynamic support is often complicated by a vascular hyporesponsiveness to exogenously administered norepinephrine. Although norepinephrine tachyphylaxis represents a significant clinical problem, the relationship between norepinephrine dosages and mean arterial pressure (MAP) in the presence of systemic inflammation is still not fully understood. This study was, therefore, designed as a prospective, controlled laboratory trial to elucidate the hemodynamic response to incremental norepinephrine doses in healthy and endotoxemic sheep. ANOVA demonstrated that a significantly higher mean infusion rate of norepinephrine was needed to increase MAP by 20 mmHg in endotoxemic versus healthy control sheep (P = 0.007). Whereas the goal-MAP was reached in 100% of healthy controls, it was achieved in only 80% during endotoxemia. Cardiac index increased significantly in healthy, but not in endotoxemic, sheep. Our findings confirm the presence of vascular hyporesponsiveness to norepinephrine in endotoxemia. In addition, this study demonstrates that the presence of systemic inflammation leads to an early hyporesponsiveness against norepinephrine which was caused by a drug-independent mechanism rather than a tachyphylaxis due to long-term administration of norepinephrine.","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 1","pages":"53-7"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907078614","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26822623","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