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Interleukin neutrophil synthesis

Inflammation is now recognized as a key process in atherogenesis [Libby, 2002]. The potential for dietary flavonoids to inhibit inflammatory activities is of particular interest. A potential anti-inflammatory feature of the flavonoids is the ability to inhibit the biosynthesis of eicosanoids. Selected phenolic acids and some flavonoids have been shown to inhibit both cyclooxygenase (COX) and 5-lipoxygenase (5-LO) pathways [Nijveldt et al., 2001 Takano-Ishikawa et al., 2006], Epicatechin and related flavonoids have been shown to inhibit the synthesis of pro-inflammatory cytokines in vitro [Sanbongi et al., 1997], and plasma metabolites of catechin and quercetin inhibit the adhesion of monocytes to cultured endothelial cells [Koga and Meydani, 2001]. Silymarin has been shown to inhibit the production of inflammatory cytokines, such as interleukin-1, interferon-, and tumor necrosis factor-a (TNFa), from macrophages and T-cells [Matsuda et al., 2005], Some flavonoids can inhibit neutrophil... [Pg.142]

Figure 4. Schematic representation of the Ca2+/CaM/CaMKK/CaMKIV/CREB/immediate early genes/IL pathway in T cells. Activation only takes place after the triple stimulation of the TCR, IL-1R and CD4/8 receptors. The end point effect of CaMKIV, which is die synthesis of interleukins and other growth factors, is common to T cells and thymocytes. Interleukins and other growth factors may have an autocrine or a paracrine effect. The different pathways included here have been addressed using Camk4-/- mouse models. Since die role of die CaMK cascade in hematopoietic stem cells and neutrophils is a little different, they are not included here... Figure 4. Schematic representation of the Ca2+/CaM/CaMKK/CaMKIV/CREB/immediate early genes/IL pathway in T cells. Activation only takes place after the triple stimulation of the TCR, IL-1R and CD4/8 receptors. The end point effect of CaMKIV, which is die synthesis of interleukins and other growth factors, is common to T cells and thymocytes. Interleukins and other growth factors may have an autocrine or a paracrine effect. The different pathways included here have been addressed using Camk4-/- mouse models. Since die role of die CaMK cascade in hematopoietic stem cells and neutrophils is a little different, they are not included here...
Clark-Lewis, I., Moser, B., Walz, A., Baggiolini, M Scott, G. J., and Aebersold, R. (1991) Chemical synthesis, purification, and characterization of two inflammatory proteins, neutrophil activating peptide I (interleukin-8) and neutrophil activating peptide 2. Biochemistry 30, 3128. [Pg.46]

One possibility is that increased synthesis is responsible for the late elevation of Mn-SOD. Recently two groups have independently reported that the mRNA of Mn-SOD is specifically induced by interleukin-1 (IL-1) or tumor necrosis factor (TNF) (M12,W10). In myocardial infarction, neutrophils and macrophages could move to the necrotized tissues following the early elevation and thus release the above cytokines. This could induce Mn-SOD synthesis in mitochondria, from... [Pg.33]

Girard D, Paquin R, Beaulieu AD Responsiveness of human neutrophils to interleukin-4 Induction of cytoskeletal rearrangements, de novo protein synthesis and delay of apoptosis. BiochemJ 1997 325 147-153. [Pg.78]


See other pages where Interleukin neutrophil synthesis is mentioned: [Pg.122]    [Pg.427]    [Pg.95]    [Pg.466]    [Pg.856]    [Pg.1391]    [Pg.233]    [Pg.392]    [Pg.692]    [Pg.462]    [Pg.70]    [Pg.124]    [Pg.309]    [Pg.216]    [Pg.140]    [Pg.3621]    [Pg.266]   
See also in sourсe #XX -- [ Pg.2 , Pg.99 , Pg.100 ]




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