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Escherichia Coli LPS (escherichia + coli_lp)
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] 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] 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] 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] | ||||||||||