Compounds > n-(3-oxododecanoyl)homoserine-lactone

n-(3-oxododecanoyl)homoserine-lactone and Pseudomonas-Infections

n-(3-oxododecanoyl)homoserine-lactone has been researched along with Pseudomonas-Infections* in 2 studies

Other Studies

2 other study(ies) available for n-(3-oxododecanoyl)homoserine-lactone and Pseudomonas-Infections

Article	Year
Development of a novel series of non-natural triaryl agonists and antagonists of the Pseudomonas aeruginosa LasR quorum sensing receptor. Bioorganic & medicinal chemistry, 2017, 01-01, Volume: 25, Issue:1 Bacterial chemical communication, through a process called quorum sensing (QS), plays a central role in infection in numerous bacterial pathogens. Quorum sensing in Pseudomonas aeruginosa employs a series of small molecule receptors including the master QS regulator, LasR. In this study we investigate a non-natural triaryl series of LasR ligands using a combination of structure activity relationship studies and computational modeling. These studies have enabled the identification of key structural requirements for ligand binding and have revealed a new strategy for inducing the therapeutically relevant antagonism of LasR. Topics: Anti-Bacterial Agents; Bacterial Proteins; Humans; Ligands; Molecular Docking Simulation; Pseudomonas aeruginosa; Pseudomonas Infections; Quorum Sensing; Structure-Activity Relationship; Trans-Activators	2017
Modulation of gene expression via disruption of NF-kappaB signaling by a bacterial small molecule. Science (New York, N.Y.), 2008, Jul-11, Volume: 321, Issue:5886 The control of innate immune responses through activation of the nuclear transcription factor NF-kappaB is essential for the elimination of invading microbial pathogens. We showed that the bacterial N-(3-oxo-dodecanoyl) homoserine lactone (C12) selectively impairs the regulation of NF-kappaB functions in activated mammalian cells. The consequence is specific repression of stimulus-mediated induction of NF-kappaB-responsive genes encoding inflammatory cytokines and other immune regulators. These findings uncover a strategy by which C12-producing opportunistic pathogens, such as Pseudomonas aeruginosa, attenuate the innate immune system to establish and maintain local persistent infection in humans, for example, in cystic fibrosis patients. Topics: 4-Butyrolactone; Adult; Animals; Cyclic AMP Response Element-Binding Protein; Cystic Fibrosis; Female; Gene Expression Regulation; Homoserine; Humans; I-kappa B Kinase; I-kappa B Proteins; Immunity, Innate; Interferon-gamma; Lipopolysaccharides; Macrophage Activation; Macrophages; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Middle Aged; NF-kappa B; NF-KappaB Inhibitor alpha; Phosphorylation; Pseudomonas aeruginosa; Pseudomonas Infections; Signal Transduction; Toll-Like Receptors; Transcription Factor RelA	2008

Article

Year

Development of a novel series of non-natural triaryl agonists and antagonists of the Pseudomonas aeruginosa LasR quorum sensing receptor.

Bioorganic & medicinal chemistry, 2017, 01-01, Volume: 25, Issue:1

Bacterial chemical communication, through a process called quorum sensing (QS), plays a central role in infection in numerous bacterial pathogens. Quorum sensing in Pseudomonas aeruginosa employs a series of small molecule receptors including the master QS regulator, LasR. In this study we investigate a non-natural triaryl series of LasR ligands using a combination of structure activity relationship studies and computational modeling. These studies have enabled the identification of key structural requirements for ligand binding and have revealed a new strategy for inducing the therapeutically relevant antagonism of LasR.

Topics: Anti-Bacterial Agents; Bacterial Proteins; Humans; Ligands; Molecular Docking Simulation; Pseudomonas aeruginosa; Pseudomonas Infections; Quorum Sensing; Structure-Activity Relationship; Trans-Activators

2017

Modulation of gene expression via disruption of NF-kappaB signaling by a bacterial small molecule.

Science (New York, N.Y.), 2008, Jul-11, Volume: 321, Issue:5886

The control of innate immune responses through activation of the nuclear transcription factor NF-kappaB is essential for the elimination of invading microbial pathogens. We showed that the bacterial N-(3-oxo-dodecanoyl) homoserine lactone (C12) selectively impairs the regulation of NF-kappaB functions in activated mammalian cells. The consequence is specific repression of stimulus-mediated induction of NF-kappaB-responsive genes encoding inflammatory cytokines and other immune regulators. These findings uncover a strategy by which C12-producing opportunistic pathogens, such as Pseudomonas aeruginosa, attenuate the innate immune system to establish and maintain local persistent infection in humans, for example, in cystic fibrosis patients.

Topics: 4-Butyrolactone; Adult; Animals; Cyclic AMP Response Element-Binding Protein; Cystic Fibrosis; Female; Gene Expression Regulation; Homoserine; Humans; I-kappa B Kinase; I-kappa B Proteins; Immunity, Innate; Interferon-gamma; Lipopolysaccharides; Macrophage Activation; Macrophages; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Middle Aged; NF-kappa B; NF-KappaB Inhibitor alpha; Phosphorylation; Pseudomonas aeruginosa; Pseudomonas Infections; Signal Transduction; Toll-Like Receptors; Transcription Factor RelA

2008