Induction of cytokine production

Okazaki M, Adachi Y, Ohno N, Yadomae T Structure-activity relationship of (1—>3) beta-D-glucans in the induction of cytokine production from macrophages, in vitro. Biol Pham Bull 1995 18 1320-1327. 

Knolle PA, Schmitt E, Jin S, Germann T, Duchmann R, Hegenbarth S, Gerken G, Lohse AW (1999) Induction of cytokine production in naive CD4(-h) T cells by antigen-presenting murine liver sinusoidal endothelial cells but failure to induce differentiaticm toward Thl cells. Gastroenterology 116 1428-1440... 

Otterlei M, Ostgaard K, Skjak-Braek G, Smidsrod O, Soon-Shiong P, Espevik T. Induction of cytokine production from human monocytes stimulated with alginate. J... 

Iwamoto M, Karachi M, Nakashima T, Kim D, Yamaguchi K, Oda T, Iwamoto Y, Muramatsu T (2005) Structure-activity relationship of alginate oligosaccharides in the induction of cytokine production from RAW264.7 cells. FEES Lett 579 4423-4429... 

Roots and aerial parts Polysaccharides Stimulation of phagocytosis Induction of cytokine production... 

Glycoproteins Induction of cytokine production Mitogenic activity... 

The key end result of TLR signalling is the induction of cytokines. Cytokines are proteins produced during an immune response that allow the maturation, activation and differentiation of effector cells in the immune system. The activation of NFkB and AP-1 by the MyD88 and the TREF dependent pathways leads to the production of proinflammatory cytokines such as IL-6, TNF-a and various chemokines. This pathway can also activate IRF-7 via TLR-7and TLR-9 allowing Type-I interferons to be produced. 

Pahan K, Sheikh FG, Namboodiri AMS and Singh 1, N-acetyl cysteine inhibits induction of NO production by endotoxin or cytokine stimulated rat peritoneal macrophages, C-6 glial cells and astrocytes. Free Radical Biology and Medicine 24(1) 39-48. 1998. 

The studies of mast cell cytokine production described above have shown that maximal induction of cytokine synthesis and release usually occurs in response to IgE-dependent activation. In common with many cell types, there is evidence that FccRI on mast cells is coupled to the phospholipase C effector system that controls two distinct signal transduction pathways, one regulated by Ca " ions and the other by protein kinase C (PKC). Exocytotic degranulation is associated with an increased cytoplasmic level of Ca ions, and activation of mast cells can be therefore achieved by the use of calcium iono-phores which raise intracellular calcium concentrations through a receptor-independent mechanism. Alternative mast cell stimuli include phorbol-12-myristate-13-acetate (PMA) which activates PKC and induces mediator secretion from basophils and rodent mast cells but not from human mast cells, and concanavalin A (Con A), a lectin which can stimulate mast cells by cross-linking of cell-bound IgE and/or cell surface glycoproteins. 

Cytokine Production/Cellular Activation TNFa and IFNy mediate the induction of other cytokines (IL-1 and IL-6) and the activation of phagocytes. It has been suggested that particle-induced expression of MIP-2 and cytokine-induced neutrophil chemoattractant CKs in the rat lung are mediated at least in part by production of TNFa. TNF is involved in control of monocyte-mediated regulation of cytokine production by T cells. Preincubation of monocytes with rTNF enhanced their ability to induce IFNy production, and TNF synthesis inhibitors decreased this induction. However, Th2 cells are stimulated in the relative absence of monocyte co-stimulatory signal(s), probably IL-6. Concerning pain responsivity, TNFa produces dose-dependent hyperalgesia mediated via the induced release of IL-lp. ... 

Singh, I., Pahan, K., Khan, M., and Singh, A.K. (1998). Cytokine-mediated induction of ceramide production is redox-sensitive. Implications to proinflammatory cytokine-mediated apoptosis in demyelinating diseases. J Biol Chem 273, 20354-62. 

Another effect of IL-1 (3 and the other proinflammatory cytokines on the central nervous system is the induction of the production of... 

The ability of xenobiotics to induce (Dastych et al., 1999) or suppress (O Keefe et al, 1992) cytokine expression has been proposed as a possible mechanism explaining their adverse effects on the immune system. To this end, ICS has been used to measure drug-induced inhibition of cytokine production, inhibition of cytokine release, induction of immunosuppressive cytokines, cytokine homeostatic maintenance, and cytokine-induced alterations in cellular activation or transcriptional mechanisms as reviewed by House (1999). 

The earliest morphological change in the sebaceous follicle is an abnormal follicular epithelial differentiation, which results in ductal hypercornification. Cornified cells in the upper section of the follicular canal become abnormally adherent. Comedones represent the retention of hyperproliferating ductal keratinoc-ytes in the duct. Several factors have been implicated in the induction of hyperproliferation sebaceous lipid composition, androgens, local cytokine production (IL-i, EGF) and bacteria (P. acnes). 

During ischaemia, NOS is activated by calcium influx or by cytokines like tumour necrosis factor (TNF) or by lipopolysaccharide (LPS) and NO is produced in excess. It has been proposed that the excitotoxic effect of glutamate, which contributes to ischaemia-induced neuronal damage, is mediated by increased production of NO via a chain of events that includes increases in intracellular calcium (via glutamate activation of NMDA receptors), calcium activation of NOS, production of NO and peroxynitrite, and induction of lipid peroxidation. In fact, N-nitro-L-atginine, a selective inhibitor of NOS, has been shown to prevent glutamate-induced neurotoxicity in cortical cell cultures (Dawson rf /., 1991). 

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