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Coli LPS (coli + lp)
Kinds of Coli LPS Selected AbstractsTREM-1 expression in macrophages is regulated at transcriptional level by NF-,B and PU.1EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 8 2007Heng Zeng Abstract Triggering receptor expressed on myeloid cells (TREM)-1 is a recently identified immunoglobulin receptor that is expressed on neutrophils and monocytes where it amplifies the acute inflammatory response to bacteria. We examined the transcriptional regulation of TREM-1 in macrophages. Treatment of RAW cells with Escherichia coli LPS or Pseudomonas aeruginosa led to the induction of TREM-1 within 1,h with an expression lasting up to at least 24,h in vitro as detected by RT-PCR. Since the promoter of TREM-1 has multiple binding sites for NF-,B and PU.1 (one of the members of the ets family of transcription factors), we investigated the role of these transcription factors in the induction of TREM-1. Treatment of cells with NF-,B inhibitors abolished the expression of message of TREM-1 induced by LPS and P.,aeruginosa. In contrast, the expression of TREM-1 was increased after stimulation with LPS or P.,aeruginosa in cells that had gene of PU.1 silenced. Additionally, over-expression of PU.1 led to inhibition of TREM-1 induction in response to LPS and P.,aeruginosa. These data suggest that both these transcription factors are involved in the expression of TREM-1. NF-,B functions as a positive regulator whereas PU.1 is a negative regulator of the TREM-1 gene. [source] Interleukin-6 Induction by Helicobacter pylori in Human Macrophages is Dependent on PhagocytosisHELICOBACTER, Issue 3 2006Stefan Odenbreit Abstract Background:, The colonization of the gastric mucosa with Helicobacter pylori is accompanied by elevated levels of proinflammatory cytokines, such as interleukin-1 (IL-1), IL-6, and IL-8. The aim of our study was to determine the mechanisms of IL-6 stimulation in phagocytes upon H. pylori infection. Materials and Methods:, We investigated the secretion of IL-6 by different professional phagocytes from murine and human origin, including granulocyte- and monocyte-like cells and macrophages derived from human peripheral blood monocytes (PBMCs). The influence of viability, phagocytosis, and the impact of different subcellular fractions of H. pylori bacteria were evaluated. Results:, IL-6 levels induced by H. pylori were low in cell lines derived from murine and human monocytes and in human granulocyte-like cells. By contrast, macrophages derived from human PBMCs were highly responsive to both H. pylori and Escherichia coli. IL-6 induction was blocked by inhibition of actin-dependent processes prior to infection with H. pylori, but not with E. coli or E. coli lipopolysaccharide (LPS). Using cell fractionation, the most activity was found in the H. pylori membrane. H. pylori LPS exhibited a 103 - to 104 -fold lower biologic activity than E. coli LPS, suggesting a minor role for toll-like receptor 4 (TLR4)-mediated signalling from the exterior. Conclusions:, From these data, we conclude that macrophages may be a major source of IL-6 in the gastric mucosa upon H. pylori infection. The IL-6 induction by H. pylori in these cells is a multifactorial process, which requires the uptake and presumably degradation of H. pylori bacteria. [source] Effect of different irrigation solutions and calcium hydroxide on bacterial LPSINTERNATIONAL ENDODONTIC JOURNAL, Issue 11 2003J. M. G. Tanomaru Abstract Aim, To evaluate the effect of biomechanical preparation with different irrigating solutions and calcium hydroxide dressing in dog root canals containing bacterial endotoxin (lipopolysaccharides; LPS). Methodology, One hundred and forty premolar roots from seven dogs were filled with Escherichia coli LPS for 10 days (three roots were lost during histological processing). The following irrigating solutions were used for biomechanical preparation: 1% (group I, n = 20), 2.5% (group II, n = 19) and 5% sodium hypochlorite (group III, n = 19), 2% chlorhexidine digluconate (group IV, n = 20) and physiological saline solution (group V, n = 19). In group VI (n = 20), the LPS solution was maintained in the root canal during the entire experiment and in group VII (n = 20), after biomechanical preparation with saline solution, the root canals were filled with a calcium hydroxide dressing (Calen; control). After 60 days, the animals were sacrificed and the following parameters of periapical disease were evaluated: (a) inflammatory infiltrate, (b) periodontal ligament thickness, (c) cementum resorption and (d) bone resorption. Scores were given and data were analysed statistically with the Kruskal,Wallis and Dunn tests (P < 0.05). Results, Histopathological evaluation showed that groups I,VI had more inflammatory infiltrate, greater periodontal ligament thickening and greater cementum and bone resorption (P < 0.05) compared to group VII, which received the calcium hydroxide intracanal dressing. Conclusions, Biomechanical preparation with the irrigating solutions did not inactivate the effects of the endotoxin but the calcium hydroxide intracanal dressing did appear to inactivate the effects induced by the endotoxin in vivo. [source] Atomic force microscopy study of the role of LPS O-antigen on adhesion of E. coliJOURNAL OF MOLECULAR RECOGNITION, Issue 5 2009Joshua Strauss Abstract The O-antigen is a highly variable component of the lipopolysaccharide (LPS) among Escherichia coli strains and is useful for strain identification and assessing virulence. While the O-antigen has been chemically well characterized in terms of sugar composition, physical properties such as O-antigen length of E. coli LPS have not been well studied, even though LPS length is important for determining binding of bacteria to biomolecules and epithelial cells. Atomic force microscopy (AFM) was used to characterize the physicochemical properties of the LPS of eight E. coli strains. Steric repulsion between the AFM tip (silicon nitride) and the E. coli cells was measured and modeled, to determine LPS lengths for three O157 and two O113 E. coli strains, and three control (K12) strains that do not express the O-antigen. For strains with an O-antigen, the LPS lengths ranged from 17,±,10 to 37,±,9,nm, and LPS length was positively correlated with the force of adhesion (Fadh). Longer lengths of LPS may have allowed for more hydrogen bonding between the O-antigen and silanol groups of the AFM silicon nitride tip, which controlled the magnitude of Fadh. For control strains, LPS lengths ranged from 3,±,2 to 5,±,3,nm, and there was no relationship between LPS length and adhesion force between the bacterium and the silicon nitride tip. In the absence of the O-antigen, we attributed Fadh to electrostatic interactions with lipids in the bacterial membrane. Copyright © 2009 John Wiley & Sons, Ltd. [source] Ethanol Exposure Impairs LPS-Induced Pulmonary LIX Expression: Alveolar Epithelial Cell Dysfunction as a Consequence of Acute IntoxicationALCOHOLISM, Issue 2 2009James E. Walker Jr Background:, Alcohol intoxication impairs innate immune responses to bacterial pneumonia, including neutrophil influx. Lipopolysaccharide (LPS)-induced chemokine (LIX or CXCL5) is a recently described chemokine produced by type-II alveolar epithelial (AE2) cells which facilitates neutrophil recruitment. The effect of acute alcohol intoxication on AE2 cell expression of LIX is unknown. Methods:, C57BL/6 mice were given an intraperitoneal (i.p.) injection of ethanol (4 g/kg) or saline 30 minutes prior to intratracheal (i.t.) injection with 10 ,g Escherichia coli LPS. In vitro stimulation of primary AE2 cells or murine AE2 cell line MLE-12 was performed with LPS and tumor necrosis factor-alpha (TNF-,). Results:, LIX protein is readily detectable in the lung but not in plasma following LPS administration, demonstrating "compartmentalization" of this chemokine during pulmonary challenge. In contrast to the CXC chemokines keratinocyte-derived chemokine and macrophage inflammatory protein-2, which are abundantly expressed in both lung tissue and alveolar macrophages, LIX expression is largely confined to the lung parenchyma. Compared to controls, intoxicated animals show a decrease in LIX and neutrophil number in bronchoalveolar lavage fluid following LPS challenge. Ethanol inhibits LIX at the transcriptional level. In vitro studies show that LPS and TNF-, are synergistic in inducing LIX by either primary AE2 or MLE-12 cells. Acute ethanol exposure potently and dose-dependently inhibits LIX expression by AE2 cells. Activation of nuclear factor-,B is critical to LIX expression in MLE-12 cells, and acute ethanol treatment interferes with early activation of this pathway as evidenced by impairing phosphorylation of p65 (RelA). Inhibition of p38 mitogen-activated protein kinase signaling, but not ERK1/2 activity, in MLE-12 cells by acute alcohol is likely an important cause of decreased LIX expression during challenge. Conclusions:, These data demonstrate direct suppression of AE2 cell innate immune function by ethanol and add to our understanding of the mechanisms by which acute intoxication impairs the lung's response to microbial challenge. [source] Ecabet sodium attenuates reactive oxygen species produced by neutrophils after priming with bacterial lipopolysaccharidesLUMINESCENCE: THE JOURNAL OF BIOLOGICAL AND CHEMICAL LUMINESCENCE, Issue 6 2003Wataru Munakata Abstract The pathogenic roles of reactive oxygen species (ROS) have been implicated in ulcerative colitis (UC). The aim of this study was to examine the effects of ecabet sodium on ROS produced by human neutrophils, particularly after being primed by bacterial lipopolysaccharides (LPS). Neutrophils were isolated from six healthy volunteers. Each well of a 96-well microplate received neutrophil suspension (1.0 × 105 cells) and the plates were incubated at 37°C for 30 min with or without E. coli LPS (f.c. 0.001 ng/µL). Ecabet sodium (f.c. 0,5.0 mg/mL) was added before starting or after finishing the incubation. Neutrophils were stimulated by opsonized zymosan (OZ; 1.0 mg/mL) or calcium ionophore (A21837; 0.3 µmol/L) and luminol-dependent chemiluminescence response was measured using a Lumi Box H-1000. Ecabet sodium attenuated ROS production at a concentration of 5.0 mg/mL (p < 0.05) in LPS-primed neutrophils. However, attenuating effects were not significantly different when ecabet sodium was added before or after the incubation with E. coli LPS. Ecabet sodium may have some attenuating effects on ROS produced by human neutrophils even after neutrophils are primed by bacterial LPS. These results may explain, in part, the therapeutic effects of ecabet sodium for UC. Copyright © 2003 John Wiley & Sons, Ltd. [source] Changes in lipopolysaccharide structure induce the ,E -dependent response of Escherichia coliMOLECULAR MICROBIOLOGY, Issue 5 2005Christina Tam Summary The envelope of Escherichia coli is composed of an asymmetric lipid bilayer containing lipopolysaccharide, phospholipid and outer membrane proteins (OMPs). Physical and chemical stresses impact on the integrity of the outer membrane envelope and trigger the ,E -dependent response, whereby E. coli activates the expression of genes that increase its capacity for folding OMPs and synthesizing lipopolysaccharide (LPS). While it has already been appreciated that misfolded OMPs induce the ,E response, a role for LPS in activating this pathway was hitherto unknown. Here we show that ammonium metavandate (NH4VO3) induces multiple changes in E. coli LPS structure and activates the ,E -dependent response without altering OMP. One such NH4VO3 -mediated LPS decoration, the CrcA/PagP-catalysed addition of palmitate to lipid A, appeared to be alone sufficient to activate transcription at ,E -dependent promoters. Furthermore, reduced acylation of LPS, caused by htrB or msbB mutations, also resulted in a constitutive expression of the ,E regulon above wild-type levels. Production of these aberrant outer membrane lipids did not noticeably affect the composition or the amount of OMPs. A model is proposed whereby structural intermediates of the LPS biosynthetic pathway or modified LPS molecules may function as signals that activate the ,E response. [source] Nitric oxide production by a murine macrophage cell line (RAW264.7) stimulated with lipopolysaccharide from Actinobacillus actinomycetemcomitansMOLECULAR ORAL MICROBIOLOGY, Issue 2 2002W. Sosroseno The aim of this study was to determine whether Actinobacillus actinomycetemcomitans lipopolysaccharide (LPS- A. actinomycetemcomitans) could stimulate a murine macrophage cell line (RAW264.7 cells) to produce nitric oxide (NO). The cells were treated with LPS- A. actinomycetemcomitans or Escherichia coli LPS (LPS- Ec) for 24 h. The effects of NG -monomethyl-L-arginine (NMMA), polymyxin B and cytokines (IFN-,, TNF-,, IL-4 and IL-12) on the production of NO were also determined. The role of protein tyrosine kinase, protein kinase C and microtubulin organization on NO production were assessed by incubating RAW264.7 cells with genistein, bisindolylmaleide and colchicine prior to LPS- A. actinomycetemcomitans stimulation, respectively. NO levels from the culture supernatants were determined by the Griess reaction. The results showed that LPS- A. actinomycetemcomitans stimulated NO production by RAW264.7 cells in a dose-dependent manner, but was slightly less potent than LPS- Ec. NMMA and polymyxin B blocked the production of NO. IFN-, and IL-12 potentiated but IL-4 depressed NO production by LPS- A. actinomycetemcomitans -stimulated RAW264.7 cells. TNF-, had no effects on NO production. Genistein and bisindolylmalemaide, but not colchicine, reduced the production of NO in a dose-dependent mechanism. The results of the present study suggest that A. actinomycetemcomitans LPS, via the activation of protein tyrosine kinase and protein kinase C and the regulatory control of cytokines, stimulates NO production by murine macrophages. [source] IL1,- and LPS-induced serotonin secretion is increased in EC cells derived from Crohn's diseaseNEUROGASTROENTEROLOGY & MOTILITY, Issue 4 2009M. Kidd Abstract, Gut mucosal enterochromaffin (EC) cells are regarded as key regulators of intestinal motility and fluid secretion via secretion of serotonin (5HT), are increased in numbers in mucosal inflammation and located in close proximity to immune cells. We examined whether interleukin (IL)1, and Escherichia coli lipopolysaccharide (LPS) induced EC cell 5HT release through Toll-like/IL-1 (TIL) receptor activation, nuclear factor kappa B (NF,B) and mitogen-activated protein kinase (MAPK) phosphorylation and evaluated whether somatostatin could inhibit this phenomenon. Pure (>98%) human intestinal EC cells were isolated by fluorescent activated cell sorting from preparations of normal (n = 5) and Crohn's colitis (n = 6) mucosa. 5HT release was measured (ELISA), and NF,B and ERK phosphorylation quantitated (ELISA) in response to IL1, and LPS. 5HT secretion was increased by both E. coli LPS (EC50 = 5 ng mL,1) and IL1, (EC50 = 0.05 pmol L,1) >2-fold (P < 0.05) in Crohn's EC cells compared with normal EC cells. Secretion was reversible by the TLR4 antagonist, E. coli K12 LPS (IC50 = 12 ng mL,1) and the IL1, receptor antagonist (ILRA; IC50 = 3.4 ng mL,1). IL1, caused significant (P < 0.05) NF,B and MAPK phosphorylation (40,55%). The somatostatin analogue, lanreotide inhibited IL1,-stimulated secretion in Crohn's (IC50 = 0.61 nmol L,1) and normal EC cells (IC50 = 1.8 nmol L,1). Interleukins (IL1,) and bacterial products (E. coli LPS) stimulated 5HT secretion from Crohn's EC cells via TIL receptor activation (TLR4 and IL1,). Immune-mediated alterations in EC cell secretion of 5HT may represent a component of the pathogenesis of abnormal bowel function in Crohn's disease. Inhibition of EC cell-mediated 5HT secretion may be an alternative therapeutic strategy in the amelioration of inflammatory bowel disease symptomatology. [source] Hierarchical gene expression profiles of HUVEC stimulated by different lipid A structures obtained from Porphyromonas gingivalis and Escherichia coliCELLULAR MICROBIOLOGY, Issue 4 2007Casey Chen Summary The ability of lipid A structural variants to elicit unique endothelial cell gene expression was examined by measuring global gene expression profiles in human umbilical cord vein endothelial cells (HUVEC) using Affymetrix full genome chips. Two lipid A structural variants obtained from Porphyromonas gingivalis designated PgLPS1435/1449 and PgLPS1690 as well as LPS obtained from Escherichia coli wild type and an E. coli msbB mutant (missing myristic acid in the lipid A) were examined. Each of these lipid A structures has been shown to interact with TLR4; however, PgLPS1435/1449 and E. coli msbB LPS have been shown to be TLR4 antagonists while PgLPS1690 and wild-type E. coli LPS are TLR4 agonists. It was found that PgLPS1435/1449 and PgLPS1690 as well as E. coli msbB LPS activated a subset of those genes significantly transcribed in response to E. coli wild-type LPS. Furthermore, the subset of genes expressed in response to the different lipid A structural forms were those most significantly activated by wild-type E. coli LPS demonstrating a hierarchy in TLR4-dependent endothelial cell gene activation. A unique gene expression profile for the weak TLR4 agonist PgLPS1690 was observed and represents a TLR4 hierarchy in endothelial cell gene activation. [source] | ||||||||||||||||