Niacin and its metabolites as master regulators of macrophage activation

Journal of Nutritional Biochemistry

Volumn 39, Issue , 2017, Pages 40-47

  Montserrat de la Paz, Sergio ^a   Naranjo, M Carmen ^a   Lopez, Sergio ^a   Abia, Rocio ^a   Muriana, Francisco J Garcia ^a   Bermudez, Beatriz ^b  

^a INSTITUTO DE LA GRASA   (Spain)

^b UNIVERSITY OF SEVILLE   (Spain)

Author keywords

Macrophages; Monocytes; Niacin; Nicotinamide; Nicotinuric acid; Polarization

Indexed keywords

INDUCIBLE NITRIC OXIDE SYNTHASE; LIPOPOLYSACCHARIDE; N METHYL 2 PYRIDONE 5 CARBOXAMIDE; NICOTINAMIDE; NICOTINIC ACID; NICOTINIC ACID DERIVATIVE; NICOTINURIC ACID; NITRIC OXIDE; REACTIVE OXYGEN METABOLITE; UNCLASSIFIED DRUG; ANTIINFLAMMATORY AGENT; ANTIOXIDANT; N-METHYL-2-PYRIDONE-5-CARBOXAMIDE; NOS2 PROTEIN, HUMAN; PYRIDONE DERIVATIVE;

ANTIINFLAMMATORY ACTIVITY; ANTIOXIDANT ACTIVITY; ARTICLE; CELL MATURATION; CELL PLASTICITY; CELL POLARITY; CONTROLLED STUDY; DRUG EFFECT; DRUG MECHANISM; FLOW CYTOMETRY; HUMAN; HUMAN CELL; IMMUNOCOMPETENCE; IN VITRO STUDY; INFLAMMATION; MACROPHAGE; MACROPHAGE ACTIVATION; METABOLITE; MONOCYTE; NUCLEAR REPROGRAMMING; OXIDATIVE STRESS; QUANTITATIVE ANALYSIS; REAL TIME POLYMERASE CHAIN REACTION; WESTERN BLOTTING; CELL DIFFERENTIATION; CELL SURVIVAL; DRUG EFFECTS; GENETICS; METABOLISM;

ANTI-INFLAMMATORY AGENTS; ANTIOXIDANTS; CELL DIFFERENTIATION; CELL SURVIVAL; HUMANS; MACROPHAGE ACTIVATION; MONOCYTES; NIACIN; NIACINAMIDE; NICOTINIC ACIDS; NITRIC OXIDE SYNTHASE TYPE II; OXIDATIVE STRESS; PYRIDONES; REACTIVE OXYGEN SPECIES; REAL-TIME POLYMERASE CHAIN REACTION;

EID: 84992517858     PISSN: 09552863     EISSN: 18734847     Source Type: Journal    
DOI: 10.1016/j.jnutbio.2016.09.008     Document Type: Article

References (47)

1. [1] EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA), European Food Safety Authority (EFSA), Scientific opinion on dietary reference values for niacin. EFSA J, 12(7), 2014, 3759.
2. [2] Sando, K.R., Knight, M., Nonstatin therapies for management of dyslipidemia: a review. Clin Ther 37 (2015), 2153–2179.
3. [3] Canner, P.L., Furberg, C.D., McGovern, M.E., Benefits of niacin in patients with versus without the metabolic syndrome and healed myocardial infarction (from the coronary drug project). Am J Cardiol 97 (2006), 477–479.
4. [4] Phan, B.A., Moore, A.B., Davis, J., Pollan, L.J., Neradilek, B., Brown, B.G., et al. Prolonged combination lipid therapy is associated with reduced carotid intima-media thickness: a case–control study of the 20-year familial atherosclerosis treatment — observational study (FATS-OS). J Clin Lipidol 8 (2014), 489–493.
5. [5] White, C.R., Goldberg, D., Anantharamaiah, G.M., Recent developments in modulating atherogenic lipoproteins. Curr Opin Lipidol 26 (2015), 369–375.
6. [6] Yadav, R., Liu, Y., Kwok, S., Hama, S., France, M., Eatough, R., et al. Effect of extended-release niacin on high-density lipoprotein (HDL) functionality, lipoprotein metabolism, and mediators of vascular inflammation in statin-treated patients. J Am Heart Assoc, 4, 2015, e001508.
7. [7] Feingold, K.R., Moser, A., Shigenaga, J.K., Grunfeld, C., Inflammation stimulates niacin receptor (GPR109A/HCA2) expression in adipose tissue and macrophages. J Lipid Res 55 (2014), 2501–2508.
8. [8] Mullangi, R., Srinivas, N.R., Niacin and its metabolites: role of LC–MS/MS bioanalytical methods and update on clinical pharmacology. An overview. Biomed Chromatogr 25 (2011), 218–237.
9. [9] Liu, M., Zhang, D., Wang, X., Zhang, L., Han, J., Yang, M., et al. Simultaneous quantification of niacin and its three main metabolites in human plasma by LC–MS/MS. J Chromatogr B Analyt Technol Biomed Life Sci 904 (2012), 107–114.
10. [10] Cooper, D.L., Murrell, D.E., Roane, D.S., Harirforoosh, S., Effects of formulation design on niacin therapeutics: mechanism of action, metabolism, and drug delivery. Int J Pharm 490 (2015), 55–64.
11. [11] Montserrat- de la Paz, S., de la Puerta, R., Fernandez-Arche, A., Quilez, A.M., Muriana, F.J., Garcia-Gimenez, M.D., et al. Pharmacological effects of mitraphylline from Uncaria tomentosa in primary human monocytes: skew toward M2 macrophages. J Ethnopharmacol 170 (2015), 128–135.
12. [12] Ziegler-Heitbrock, L., Ancuta, P., Crowe, S., Dalod, M., Grau, V., Hart, D.N., et al. Nomenclature of monocytes and dendritic cells in blood. Blood 116 (2010), e74–e80.
13. [13] Ingersoll, M.A., Spanbroek, R., Lottaz, C., Gautier, E.L., Frankenberger, M., Hoffmann, R., Comparison of gene expression profiles between human and mouse monocyte subsets. Blood 115 (2010), e10–e19.
14. [14] Wong, K.L., Yeap, W.H., Tai, J.J., Ong, S.M., Dang, T.M., Wong, S.C., The three human monocyte subsets: implications for health and disease. Immunol Res 53 (2012), 41–57.
15. [15] Shantsila, E., Wrigley, B., Tapp, L., Apostolakis, S., Montoro-Garcia, S., Drayson, M.T., et al. Immunophenotypic characterization of human monocyte subsets: possible implications for cardiovascular disease pathophysiology. J Thromb Haemost 9 (2011), 1056–1066.
16. [16] Cros, J., Cagnard, N., Woollard, K., Patey, N., Zhang, S.Y., Senechal, B., et al. Human CD14dim monocytes patrol and sense nucleic acids and viruses via TLR7 and TLR8 receptors. Immunity 33 (2010), 375–386.
17. [17] Italiani, P., Boraschi, D., From monocytes to M1/M2 macrophages: phenotypical vs functional differentiation. Front Immunol, 5, 2014, 514.
18. [18] Zawada, A.M., Rogacev, K.S., Schirmer, S.H., Sester, M., Böhm, M., Fliser, D., et al. Monocyte heterogeneity in human cardiovascular disease. Immunobiology 217 (2012), 1273–1284.
19. [19] Gordon, S., Martinez, F.O., Alternative activation of macrophages: mechanism and functions. Immunity 32 (2010), 593–604.
20. [20] Benoit, M., Desnues, B., Mege, J.L., Macrophage polarization in bacterial infections. J Immunol 181 (2008), 3733–3739.
21. [21] Porta, C., Riboldi, E., Ippolito, A., Sica, A., Molecular and epigenetic basis of macrophage polarized activation. Semin Immunol 27 (2015), 237–248.
22. [22] Wanders, D., Graff, E.C., White, B.D., Judd, R.L., Niacin increases adiponectin and decreases adipose tissue inflammation in high fat diet-fed mice. PLoS One, 8, 2013, e71285.
23. [23] Benjó, A.M1., Maranhão, R.C., Coimbra, S.R., Andrade, A.C., Favarato, D., Molina, M.S., et al. Accumulation of chylomicron remnants and impaired vascular reactivity occur in subjects with isolated low HDL cholesterol: effects of niacin treatment. Atherosclerosis 187 (2006), 116–122.
24. [24] Shapiro, M.D., Fazio, S., From lipids to inflammation: new approaches to reducing atherosclerotic risk. Circ Res 118:4 (2016), 732–749.
25. [25] Su, G1., Sun, G2., Liu, H1., Shu, L1., Zhang, J1., Guo, L1., et al. Niacin suppresses progression of atherosclerosis by inhibiting vascular inflammation and apoptosis of vascular smooth muscle cells. Med Sci Monit 21 (2015), 4081–4089.
26. [26] Kuvin, J.T., Dave, D.M., Sliney, K.A., Mooney, P., Patel, A.R., Kimmelstiel, C.D., et al. Effects of extended release niacin on lipoprotein particle size, distribution and inflammatory markers in patients with coronary artery disease. Am J Cardiol 98 (2006), 743–745.
27. + monocytes as a third monocyte subset. Blood 118 (2011), 50–61.
28. [28] Ka, S.O., Song, M.Y., Bae, E.J., Park, B.H., Myeloid SIRT1 regulates macrophage infiltration and insulin sensitivity in mice fed a high-fat diet. J Endocrinol 224 (2015), 109–118.
29. [29] Yang, J., Zhang, L., Caijia, Y., Yang, X.F., Wang, H., Monocyte and macrophage differentiation: circulation inflammatory monocyte as biomarker for inflammatory diseases. Biomark Res, 2, 2014, 1.
30. [30] Murray, P.J., Wynn, T.A., Protective and pathogenic functions of macrophage subsets. Nat Rev Immunol 11 (2011), 723–737.
31. [31] Benavente, C.A., Jacobson, E.L., Niacin restriction upregulates NADPH oxidase and reactive oxygen species (ROS) in human keratinocytes. Free Radic Biol Med 44 (2008), 527–537.
32. [32] Slominska, E.M., Smolenski, R.T., Osborne, F., Swierczynski, J., Yacoub, M.H., The effect of N-methyl-2-pyridone-5-carboxamide — a nicotinamide catabolite on poly ADP-rybosylation and oxidative stress injury in endothelial cells. Nucleosides Nucleotides Nucleic Acids 24 (2005), 259–262.
33. [33] Digby, J.E., McNeill, E., Dyar, O.J., Lam, V., Greaves, D.R., Choudhury, R.P., Anti-inflammatory effects of nicotinic acid in adipocytes demonstrated by suppression of fractalkine, RANTES, and MCP-1 and upregulation of adiponectin. Atherosclerosis 209 (2010), 89–95.
34. [34] Qureshi, A.A., Guan, X.Q., Reis, J.C., Papasian, C.J., Jabre, S., Morrison, D.C., et al. Inhibition of nitric oxide and inflammatory cytokines in LPS-stimulated murine macrophages by resveratrol, a potent proteasome inhibitor. Lipids Health Dis, 11, 2012, 76.
35. [35] Huang, H., Koelle, P., Fendler, M., Schroettle, A., Czihal, M., Hoffmann, U., et al. Niacin reverses migratory macrophage foam cell arrest mediated by oxLDL in vitro. PLoS One, 9, 2014, 114643.
36. [36] Zhang, J., Rane, G., Dai, X., Shanmugam, M.K., Arfuso, F., Samy, R.P., et al. Ageing and the telomere connection: an intimate relationship with inflammation. Ageing Res Rev 25 (2016), 55–69.
37. −/− mice: a comparison with nicotinic acid. J Pharmacol Exp Ther, 2015 [pii: jpet.115.228643].
38. [38] Lipszyc, P.S., Cremaschi, G.A., Zorrilla-Zubilete, M., Bertolino, M.L., Capani, F., Genaro, A.M., et al. Niacin modulates pro-inflammatory cytokine secretion. A potential mechanism involved in its anti-atherosclerotic effect. Open Cardiovasc Med J 7 (2013), 90–98.
39. [39] Fiedorowicz, J.G., Prossin, A.R., Johnson, C.P., Christensen, G.E., Magnotta, V.A., Wemmie, J.A., Peripheral inflammation during abnormal mood states in bipolar I disorder. J Affect Disord 187 (2015), 172–178.
40. [40] Ballak, D.B., van Essen, P., van Diepen, J.A., Jansen, H., Hijmans, A., Matsuguchi, T., et al. MAP3K8 (TPL2/COT) affects obesity-induced adipose tissue inflammation without systemic effects in humans and in mice. PLoS One, 9, 2014, e89615.
41. [41] Lagman, M., Ly, J., Saing, T., Kaur Singh, M., Vera Tudela, E., Morris, D., et al. Investigating the causes for decreased levels of glutathione in individuals with type II diabetes. PLoS One, 10, 2015, e0118436.
42. [42] Howe, L.R., Subbaramaiah, K., Hudis, C.A., Dannenberg, A.J., Molecular pathways: adipose inflammation as a mediator of obesity-associated cancer. Clin Cancer Res 19 (2013), 6074–6083.
43. [43] Si, Y., Zhang, Y., Zhao, J., Guo, S., Zhai, L., Yao, S., et al. Niacin inhibits vascular inflammation via downregulating nuclear transcription factor-κB signaling pathway. Mediators Inflamm, 263786, 2014.
44. [44] Zhou, E., Li, Y., Yao, M., Wei, Z., Fu, Y., Yang, Z., Niacin attenuates the production of pro-inflammatory cytokines in LPS-induced mouse alveolar macrophages by HCA2 dependent mechanisms. Int Immunopharmacol 23 (2014), 121–126.
45. [45] Zandi-Nejad, K., Takakura, A., Jurewicz, M., Chandraker, A.K., Offermanns, S., Mount, D., et al. The role of HCA2 (GPR109A) in regulating macrophage function. FASEB J 27 (2013), 4366–4374.
46. [46] Weiss, R., Schilling, E., Grahnert, A., Kölling, V., Dorow, J., Ceglarek, U., et al. Nicotinamide: a vitamin able to shift macrophage differentiation toward macrophages with restricted inflammatory features. Innate Immun 21 (2015), 813–826.
47. [47] Malyshev, I., Malyshev, Y., Current concept and update of the macrophage plasticity concept: intracellular mechanisms of reprogramming and M3 macrophage “switch” phenotype. Biomed Res Int, 341308, 2015.