What question did this study set out to answer?

To determine whether bacterial lipopolysaccharide utilizes interleukin-1 or tumor necrosis factor signal transduction pathways to activate NF-κB in human endothelial and monocytic cells.

March 1, 1999Journal of Biological ChemistryOpen Access

Bacterial Lipopolysaccharide Activates Nuclear Factor-κB through Interleukin-1 Signaling Mediators in Cultured Human Dermal Endothelial Cells and Mononuclear Phagocytes

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Authors

XZXiao Hui ZhangSouth China Agricultural University CKCarsten J. KirschningUniversity of Duisburg-Essen RMRoberta MancinelliCedars-Sinai Medical Center

Discussion

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Implication

In vitro study reveals that lipopolysaccharide activates NF-κB via IL-1 signaling mediators in human endothelial and monocytic cells, suggesting a shared receptor framework in sepsis response.

Key Points

To determine whether bacterial lipopolysaccharide utilizes interleukin-1 or tumor necrosis factor signal transduction pathways to activate NF-κB in human endothelial and monocytic cells.
Cultured human dermal microvessel endothelial cells (HDMEC) and THP-1 monocytic cells under stimulation with bacterial lipopolysaccharide (LPS).
Performed transient cotransfections with dominant-negative mutants of IL-1 pathway components (MyD88, IRAK, IRAK2, TRAF6) and TNF pathway components (TRAF2) to measure NF-κB-luciferase reporter activity.
Assessed surface expression of TLR2 and TLR4 and evaluated the inhibitory capacity of an IL-1 receptor antagonist.
Dominant-negative mutants of IL-1 pathway mediators (MyD88, IRAK, IRAK2, and TRAF6) strongly inhibited both IL-1- and LPS-induced NF-κB-luciferase reporter activation.
Dominant-negative TRAF2 and IL-1 receptor antagonist failed to block LPS-induced NF-κB activation.
TLR2 and TLR4 surface expression was verified on both HDMEC and THP-1 cells, supporting an IL-1 receptor/Toll-like receptor superfamily signaling mechanism.

Cite This Study

Zhang et al. (1999) studied this question.

synapsesocial.com/papers/6a0a0fc141a1eeaa0645add4 https://doi.org/10.1074/jbc.274.12.7611

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March 1, 1999Journal of Biological ChemistryOpen Access

Bacterial Lipopolysaccharide Activates Nuclear Factor-κB through Interleukin-1 Signaling Mediators in Cultured Human Dermal Endothelial Cells and Mononuclear Phagocytes

View Full Paper

Ask AI

Bookmark

Authors

XZXiao Hui ZhangSouth China Agricultural University CKCarsten J. KirschningUniversity of Duisburg-Essen RMRoberta MancinelliCedars-Sinai Medical Center

Discussion

Member takes

Implication

In vitro study reveals that lipopolysaccharide activates NF-κB via IL-1 signaling mediators in human endothelial and monocytic cells, suggesting a shared receptor framework in sepsis response.

Key Points

To determine whether bacterial lipopolysaccharide utilizes interleukin-1 or tumor necrosis factor signal transduction pathways to activate NF-κB in human endothelial and monocytic cells.
Cultured human dermal microvessel endothelial cells (HDMEC) and THP-1 monocytic cells under stimulation with bacterial lipopolysaccharide (LPS).
Performed transient cotransfections with dominant-negative mutants of IL-1 pathway components (MyD88, IRAK, IRAK2, TRAF6) and TNF pathway components (TRAF2) to measure NF-κB-luciferase reporter activity.
Assessed surface expression of TLR2 and TLR4 and evaluated the inhibitory capacity of an IL-1 receptor antagonist.
Dominant-negative mutants of IL-1 pathway mediators (MyD88, IRAK, IRAK2, and TRAF6) strongly inhibited both IL-1- and LPS-induced NF-κB-luciferase reporter activation.
Dominant-negative TRAF2 and IL-1 receptor antagonist failed to block LPS-induced NF-κB activation.
TLR2 and TLR4 surface expression was verified on both HDMEC and THP-1 cells, supporting an IL-1 receptor/Toll-like receptor superfamily signaling mechanism.

Cite This Study

Zhang et al. (1999) studied this question.

synapsesocial.com/papers/6a0a0fc141a1eeaa0645add4 https://doi.org/10.1074/jbc.274.12.7611

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