Nuclear factor kappa B, a mediator of lipopolysaccharide effects

Nuclear factor‐κB activation in human monocytes stimulated with lipopolysaccharide is inhibited by fibroblast conditioned medium and exogenous PGE2

“…Mechanisms by which LPS activates mononuclear phagocytes, its major cellular target, have not yet been completely characterized. LPS provokes multiple effects on mononuclear phagocytes including NF-KB mobilization [24], cytokine gene activation and release [25][26][27]. Several cell surface molecules such as CDI4, CDlllCDl8 are able to recognize the lipid A portion of the polysaccharide region of the LPS molecule [28,29].…”

Effect of proteasome inhibitors on monocytic IκB-α and -β depletion, NF-κB activation, and cytokine production

“…Cells of the monocytic lineage express defined sets of proinflammatory cytokines during acute and chronic inflammatory disease [1][2][3]. Besides autoregulatory loops, these cytokines exert a variety of effects on other cells involved in defense, such as lymphocytes, granulocytes, and endothelial cells.…”

“…The pleiotropic transcription factor nuclear factor-B (NF-B) has been suggested to play an important role in monocytic gene regulation [2,4,5]. Although NF-B regulatory sequences have been found in promoters or enhancers of tumor necrosis factor (TNF), interleukin-1␤ (IL-1␤), IL-6, IL-8, tissue factor, and monocyte chemotactic protein-1 [2,4,5], there is still debate concerning the extent to which NF-B is required for the expression of these genes [6][7][8].…”

“…Although NF-B regulatory sequences have been found in promoters or enhancers of tumor necrosis factor (TNF), interleukin-1␤ (IL-1␤), IL-6, IL-8, tissue factor, and monocyte chemotactic protein-1 [2,4,5], there is still debate concerning the extent to which NF-B is required for the expression of these genes [6][7][8]. In fact, the removal/mutation of the NF-B sites of the TNF promoter did reduce, but not abolish, lipopolysaccharide (LPS) induction of a reporter gene construct [8].…”

Oxidized LDL modulates activation of NFκB in mononuclear phagocytes by altering the degradation of IκBs

“…Such stimuli generally act to enhance transcription of inflammatory genes by modulating the activity of sequence-specific DNA binding factors that interact with cognate sequence motifs in target genes [19][20][21]. The B sequence motif is well documented as an important regulator of gene expression during inflammation and both LPS and the combination of IFN-␥ and interleukin-2 (IL-2) are known to stimulate B binding activities in macrophages [22][23][24][25]. The B motif is recognized by members of the Rel homology family, which includes N B1 (p50), NF B2 (p52), RelA (p65), c-Rel, and RelB [23,25].…”