THP-1 macrophages

Qiu G, Ho AC, Yu W, Hill JS (2007) Suppression of endothelial or lipoprotein lipase in THP-1 macrophages attenuates pro-inflammatory cytokine secretion. J Lipid Res 48 385-394... 

Garner B, Mellor HR, Butters TD, et al. (2002) Modulation of THP-1 macrophage and cholesterol-loaded foam cell apolipoprotein E levels by glycosphingolipids. Biochem Biophys Res Commun 290 1361-1367... 

Gaus K, Gooding 11, Dean RT, et al. (2001) A kinetic model to evaluate cholesterol efflux from THP-1 macrophages to apolipoprotein A-1. Biochemistry 40 9363-9373... 

Ocana Fuentes, A., Arranz Gutierrez, E., Senorans, F. J., and Reglero, G. (2010). Supercritical uid extraction of oregano (Origanum vulgare) essential oils Anti-in ammatory properties based an cytokine response an THP-1 macrophages. 48, 1568-1575. 

CheUat F, Grandjean-Laquerriere A, Naour RL, Fernandes J, Yahia LH, Guenounou M, Laurent-Maquin D. Metalloproteinase and cytokine production by THP-1 macrophages following exposure to chitosan-DNA nanoparticles. Biomateiials. 2005 26(9) 961-70. 

Fu Y, Luo N, Lopes-Virella MF, Garvey WT. The adipocyte lipid binding protein (ALBP/aP2) gene facilitates foam cell formation in human THP-1 macrophages. Atherosclerosis 2002 165 259-269. 

In another study, hesperetin enhanced ApoA-l-mediated cholesterol efflux in THP-1 macrophages, probably due to a greater transcription of ABCAl gene, which is critical for cholesterol metabolism. The effect of hesperetin on ABCAl-dependent cholesterol efflux may be explained in part by its LXRa and PPARy agonist action. These results indicates the potential of this flavonoid in the prevention and treatment of atherosclerosis [61]. 

FIGURE 12.10 (a) SEM image of a THP-1 cell deposited on SWNTs coated with IgG antibodies. The arrows indicate locations of polystyrene beads ingested by the cell as a test of phagocytic activity, (b) Schematic view of the interactions between a macrophage and SWNTs. (c) Electrochemical measurement with an SWNT transistor at -700 mV versus Ag/AgCl in the presence of a THP-1 macrophage. (Reproduced from Heller, I. et al., Small, 5, 2528, 2009. With permission.)... 

Pharmacodynamic evaluation of the intracellular activities of antibiotics against Staphylococcus aureus in a model of THP-1 macrophages , Antimicrob Agents Chemother, 50,841-851. 

Gieseg, S.P., Maghzal, G., and Glubb, D., Protection of erythrocytes by the macrophage synthesized antioxidant 7,8 dihydroneopterin. Free Radic. Res., 34, 123, 2001. Gieseg, S.P. and Cato, S., Inhibition of THP-1 cell-mediated low-density lipoprotein oxidation by the macrophage-synthesised pterin, 7,8-dihydroneopterin, Redox Rep., 8, 113, 2003. 

Baird, S.K. et al., OxLDL induced cell death is inhibited by the macrophage synthesised pterin, 7,8-dihydroneopterin, in U937 cells but not THP-1 cells, Biochim. Biophys. Acta 1745, 361, 2005. 

M25. Megyeri, P., Issekutz, T. B., and Issekutz, A. C. An endotoxin-induced factor distinct from interleukin-1 and tumour necrosis factor alpha produced by the THP-1 human macrophage line stimulates polymorphonuclear leukocyte infiltration in vivo. J. Leukocyte Biol. 47, 70-78 (1990). 

While ASMase-deficient mice survive lethal doses of LPS (see above), the serum levels of TNF-a-induced by sublethal doses of LPS are similar to those in WT mice (Haimovitz-Friedman et ak, 1997) isolated ASMase-deficient macrophages respond to LPS with a normal pattern of cytokine secretion (Manthey and Schuchman, 1998). Thus, there is no evidence that ASMase is important for LPS-induced inflammatory responses. A recent report showed that imipramine, an inhibitor of cellular ASMase activity, blocked LPS-induced TNF-a secretion from differentiated human monocyte-like THP-1 cells (Cuschieri et ak, 2007). However, in our hands imipramine has no effect on cytokine secretion from these cells or from monocytes isolated from human blood (A.Billich, unpublished observations). 

Phagocytosis of apoptotic cells by macrophages leads to the production of anti-inflammatory cytokines as a way of preventing inflammation. Kurosaka et al. [79] have demonstrated that human serum potentiates the production of two anti-inflammatory cytokines, IL-10 and TGF-J3, by both TPA-treated THP-1 cells and human monocyte-derived macrophages. This enhanced response to the presence of apoptotic cells also results in the suppression of the production of the pro-inflammatory cytokine IL-8. In addition, human IgG and FcyRI appear to be critical in triggering the production of anti-inflammatory cytokines by macrophages in response to apoptotic cells. 

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