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l homoserine/inflamación

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Objective To explore the regulatory effect of quorum sensing molecule N-3-oxodecanoyl-L-homoserine lactone (3-oxo-C10-HSL) on lipopolysaccharide (LPS)-induced inflammation in RAW264.7 macrophages. Methods RAW264.7 macrophages were divided into experimental group, control group and blank
The bacterial molecule N-3-oxo-dodecanoyl-l-homoserine lactone (C12) has critical roles in both interbacterial communication and interkingdom signaling. The ability of C12 to downregulate production of the key proinflammatory cytokine TNF-α in stimulated macrophages was suggested to contribute to
BACKGROUND Pseudomonas aeruginosa is frequently isolated from chronic wounds and causes serious infection in immunocompromised hosts. N-(3-Oxododecanoyl)-L-homoserine lactone (3-oxo-C12-HSL) is synthesized by an autoinducer synthase encoded by the bacterial lasI gene in P. aeruginosa, which
The pathogen Pseudomonas aeruginosa causes serious damage in immunocompromised patients by secretion of various virulence factors, among them the quorum sensing N-(3-oxododecanoyl)-L-homoserine lactone (3OC12) and the redox-active pyocyanin (PCN). Paraoxonase-2 (PON2) may protect against P.
Quorum-sensing systems have been reported to play a critical role in the pathogenesis of several bacterial infections. Recent data have demonstrated that Pseudomonas N-3-oxododecanoyl-L-homoserine lactone (3-oxo-C12-homoserine lactone, 3-oxo-C12-HSL), but not N-butanoyl-L-homoserine lactone

Expression of toll-like receptors in T lymphocytes stimulated with N-(3-oxododecanoyl)-L-homoserine lactone from Pseudomonas aeruginosa.

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The establishment of chronic Pseudomonas aeruginosa infections is correlated with the disturbance of the host immune system. The P. aeruginosa quorum-sensing molecule N-3-(oxododecanoyl)-L-homoserine lactone (3-O-C12-HSL) has the potential to modulate the host immune system. The immune system

N-3-(oxododecanoyl)-L-homoserine lactone promotes the induction of regulatory T-cells by preventing human dendritic cell maturation.

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N-3-(Oxododecanoyl)-L-homoserine lactone (C12) is a small bacterial signaling molecule secreted by Pseudomonas aeruginosa (PA), which activates mammalian cells through TLR4-independent mechanisms. C12 acts as an immunosuppressant and it has been shown to modulate murine bone marrow-derived dendritic
N-(3-oxododecanoyl)-l-homoserine lactone (3-oxo-C12-HSL), a quorum-sensing (QS) molecule produced by Gram-negative bacteria in the gastrointestinal tract, adversly impacts host cells. Our previous study demonstrated that 3-oxo-C12-HSL induced a decrease in cell viability via cell apoptosis and
N-3-(oxododecanoyl)-L-homoserine lactone (OdDHL), a quorum-sensing molecule of Pseudomonas aeruginosa, plays an important role in the pathogenesis of the organism through its control of virulence factor expression. Several reports have suggested that OdDHL can also directly modulate host immune

Impact of Pseudomonas aeruginosa quorum sensing signaling molecules on adhesion and inflammatory markers in endothelial cells.

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Pseudomonas aeruginosa relies on the quorum sensing (QS) signaling system as a central regulator mechanism of virulence expression that contributes to the formation and maintenance of biofilms and tolerance to conventional antimicrobials. QS Signaling molecules (QSSMs) may be recognized and may

Critical factors in the development of tumor-targeted anti-inflammatory nanomedicines.

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Tumors are complex and dynamic assemblies of different cell types within an atypical/abnormal architecture. Tumor-associated macrophages, mast cells, dendritic cells, eosinophils, fibroblasts are present in and around tumors and contribute to an abundant, deregulated and long lasting chronic

Promotion of acute-phase skin wound healing by Pseudomonas aeruginosa C4 -HSL.

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A Pseudomonas aeruginosa quorum-sensing system, which produces N-(3-oxododecanoyl)-l-homoserine lactone (3-oxo-C12 -HSL) and N-butanoyl-l-homoserine lactone (C4 -HSL), regulates the virulence factors. In our previous study, 3-oxo-C12 -HSL, encoded by lasI gene, was shown to promote wound healing.

Pseudomonas aeruginosa quorum-sensing signal molecules induce IL-8 production by human corneal epithelial cells.

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OBJECTIVE The aim of the present study was to evaluate whether the quorum-sensing molecules of Pseudomonas aeruginosa could induce the production of interleukin-8 (IL-8) in human corneal epithelial (HCE) cells in vitro. METHODS A confluent monolayer of immortalized HCE cells was treated with 12.5 to
Quorum sensing (QS) is a type of cell-to-cell communication. The Pseudomonas aeruginosa QS molecule N-3-(oxododecanoyl)-L-homoserine lactone (3-o-C12-HSL) has the potential to modulate the immune system of its host. However, the mechanism of that activity is yet to be fully characterized. To be able

Immunomodulatory effects of Pseudomonas aeruginosa quorum sensing small molecule probes on mammalian macrophages.

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Pseudomonas aeruginosa produces the quorum sensing signalling molecule N-(3-oxododecanoyl)-L-homoserine lactone (OdDHL). This natural product not only coordinates production of virulence factors by the bacterium, but also has immunomodulatory effects on the host organism. Immunomodulatory small
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