Tumor necrosis factor-alpha cell culture

Pulliam L, West D, Haigwood N, Swanson RA (1993) HIV-1 envelope gpl20 alters astrocytes in human brain cultures. AIDS Res Hum Retroviruses 9 439 44 Pulliam L, Zhou M, Stubblebine M, Bitler CM (1998) Differential modulation of cell death proteins in human brain cells by tumor necrosis factor alpha and platelet activating factor. J Neurosci Res 54 530-538... 

Some new materials perspective for advanced biomedical technologies, especially carbon nanoparticles like fullerenes, are potentially mutagenic, carcinogenic and immunogenic [16,65], Therefore, standard tests of the morphological transformation of Syrian hamster embryonic cells in cultures on these materials (described in detail by [68,69]) can be performed. Immune activation of bone and vascular cells on the materials can be estimated by increased concentration of immunoglobulin and selectin adhesion molecules (ICAM-1, VCAM-1, ELAM-1), which bind cells of the immune system [15,16,18,19,23], as well as by the production of cytokines, such as tumor necrosis factor alpha or interleukins beta [55],... 

The LBP facilitates the binding of LPS or GNB to phagocytes (Tobias et al., 1988 Corriveau and Danner, 1993 Yu and Wright, 1996). The enhanced interaction between LPS and phagocytes causes a marked increase in cell activation. Addition of small amounts of LBP to cultured macrophages increases by 100-fold the ability of LPS to induce the production of tumor necrosis factor alpha (TNF-a), a potent... 

Chao CC, Hu S (1994) Tumor necrosis factor-alpha potendates glutamate rreurotoxicity irr human fetal brain cell cultures. Dev Neu-rosci 16 172-179. 

Kras, K.M., Hausman, D.B., and Martin, R.J. 2000. Tumor necrosis factor-alpha stimulates cell proliferation in adipose tissue-derived stromal-vascular cell culture Promotion of adipose tissue expansion by paracrine growth factors. Obes. Res. 8, 186-193. 

Kawase E, Yamamoto H, Hashimoto K, Nakatsuji N (1994) Tumor necrosis factor-alpha (TNF-alpha) stimulates proliferation of mouse primordial germ cells in culture. Dev Biol 161(l) 91-95. 

The production of inflammatory cytokines and cell adhesion molecules (CAMs) by the arterial endothelium are key cellular events involved in the development of atherosclerosis. Activation of the endothelium results in the release of vascular cytokines such as interleukin-1 (IL-la) and tumor necrosis factor alpha (TNF-a). These cytokines induce the expression of CAMs such as intracellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1), which, together with activated monocyte chemoattractant protein-1 (MCP-1), recruit monocytes through the vascular wall, where they are involved in foam cell formation. The nuclear transcription factor, NF-kB, is a mediator in TNF-a-induced expression of cell adhesion molecules and MCP. NF-kB is activated by an atherogenic diet (Liao et al. 1993) and oxidized LDL (Brand et al. 1997), and activation is inhibited by various antioxidants (Kunsch and Medford 1999). Therefore it is of particular interest that GEN attenuated NF-kB DNA binding and TNF-a release in human monocytes (Shames et al. 1999). A small, uncontrolled pilot study ( = 6) found that GEN, but not DAI, inhibited TNF-a-induced NF-kB activation in ex vivo human lymphocytes following consumption of 100 mg isoflavones/day for 3 weeks, as well as in cultured human... 

Sallusto F, Lanzavecchia A. Efficient presentation of soluble antigen by cultured human dendritic cells is maintained by granulocyte/macrophage colony-stimulating factor plus interleukin 4 and downregulated by tumor necrosis factor alpha. J Exp Med 1994 179 1109-1118. 

Monney, L., Ohvier, R., Otter, 1., Jansen, B., Poirier, GG., and Bomer, C., 1998, Role ofan acidic compartment in tumor-necrosis-factor-a-induced production of ceramide, activation of caspase-3 and apoptosis. Eur. J. Biochem. 251 295-303 Morrison, H., Jemstrom, B., Nordenskjdld, M., Thor, H., and Orrenius, S., 1984, Induction of DNA damage by menadione (2-methyl-l,4-naphthoquinone) in primary cultures of rat hepatocytes. Biochem. Pharmacol. 33 1763-1769 Neuzil, J., Svensson, 1., Weber, T, Weber, C., and Brunk, U.T., 1999, alpha-tocopheryl succinate-induced apoptosis in Jurkat T cells involves caspase-3 activation, and both lysosomal and mitochondrial destabilisation. FEES Lett. 445 295-300 Ngo, E.O., Nutter, L.M., Sura, T., and Gutierrez, P. L., 1998, Induction ofp53 by the... 

The studies mentioned above indicate that bromelain has a certain cytotoxic potential. It remains an open question whether the observed antineoplastic effects of bromelain preparations reside in the proteolytic enzyme or in some or more other components of the mixture. Before the work of Maurer et al. [104] and of Batkin et al. [105], the antitumor activity of bromelain was explained primarily by its fibrinolytic and platelet aggregation inhibitory activity, which is believed to interfere with the fibrin and coagulation features of tumor cells [2], More recently, Desser and Rehberger [107] demonstrated that bromelain stimulates the production of alpha tumor necrosis factor in human peripheral blood mononuclear cell cultures in a time-dependent manner. Immunomodulation, especially the release of cytokines, is believed to be responsible for the possible therapeutic potential of bromelain. However, further experimental evidence is necessary, first, to prove the antineoplastic action of the proteolytic enzyme, and second, to demonstrate that bromelain in vivo is a valuable therapeutic agent in humans. 

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