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Current Heart Failure Reports

Erschienen in:

01.06.2015 | Comorbidities of Heart Failure (CE Angermann, Section Editor)

Cellular Immunity and Cardiac Remodeling After Myocardial Infarction: Role of Neutrophils, Monocytes, and Macrophages

verfasst von: Hisahito Shinagawa, Stefan Frantz

Erschienen in: Current Heart Failure Reports | Ausgabe 3/2015

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Abstract

Today, innate immunity is recognized as an important pathophysiologic factor and therapeutic target for cardiac remodeling after myocardial infarction (MI). The innate immune system exerts its function via soluble and cellular components. Recently, function and kinetics of immune cells after MI have been clarified using new innovative technology. Therefore, herein, we will discuss the function of neutrophils, monocytes, and macrophages in the pathophysiology of cardiac remodeling after MI in basic as well as clinical science.

Hofmann U, Frantz S. How can we cure a heart “in flame”? A translational view on inflammation in heart failure. Basic Res Cardiol. 2013;108:356. doi:10.1007/s00395-013-0356-y.CrossRefPubMedCentralPubMed

Mann DL, McMurray JJ, Packer M, Swedberg K, Borer JS, Colucci WS, et al. Targeted anticytokine therapy in patients with chronic heart failure: results of the Randomized Etanercept Worldwide Evaluation (RENEWAL). Circulation. 2004;109:1594–602.CrossRefPubMed

3.••

Frantz S, Nahrendorf M. Cardiac macrophages and their role in ischaemic heart disease. Cardiovasc Res. 2014;102:240–8. doi:10.1093/cvr/cvu025. This review summarized macrophage fate and function in steady status and ischemic heart diseases including interactions with other organs.CrossRefPubMedCentralPubMed

Ma Y, Yabluchanskiy A, Lindsey ML. Neutrophil roles in left ventricular remodeling following myocardial infarction. Fibrogenesis Tissue Repair. 2013;6:11. doi:10.1186/1755-1536-6-11.CrossRefPubMedCentralPubMed

Di Filippo C, Rossi F, D’Amico M. Targeting polymorphonuclear leukocytes in acute myocardial infarction. Sci World J. 2007;7:121–34.CrossRef

Akpek M, Kaya MG, Lam YY, Sahin O, Elcik D, Celik T, et al. Relation of neutrophil/lymphocyte ratio to coronary flow to in-hospital major adverse cardiac events in patients with ST-elevated myocardial infarction undergoing primary coronary intervention. Am J Cardiol. 2012;6:621–7. doi:10.1016/j.amjcard.2012.04.041.CrossRef

Jolly SR, Kane WJ, Hook BG, Abrams GD, Kunkel SL, Lucchesi BR. Reduction of myocardial infarct size by neutrophil depletion: effect of duration of occlusion. Am Heart J. 1986;112:682–90. doi:10.1016/0002-8703(86)90461-8.CrossRefPubMed

Frantz A, Bauersachs J, Ertl G. Post-infarct remodelling: contribution of wound healing and inflammation. Cardiovasc Res. 2009;81:474–81. doi:10.1093/cvr/cvn292.CrossRefPubMedCentralPubMed

Timmers L, Pasterkamp G, de Hoog VC, Arslan F, Appelman Y, de Kleijn DP. The innate immune response in reperfused myocardium. Cardiovasc Res. 2012;94:276–83. doi:10.1093/cvr/cvs018.CrossRefPubMed

10.

Prince LR, Whyte MK, Sabroe I, Parker LC. The role of TLRs in neutrophil activation. Curr Opin Pharmacol. 2011;11:397–403. doi:10.1016/j.coph.2011.06.007.CrossRefPubMed

11.

Oyama J, Blais Jr C, Liu X, Pu M, Kobzik L, Kelly RA, et al. Reduced myocardial ischemia-reperfusion injury in toll-like receptor 4-deficient mice. Circulation. 2004;109:784–9.CrossRefPubMed

12.

Arslan F, Smeets MB, O’Neill LA, Keogh B, McGuirk P, Timmers L, et al. Myocardial ischemia/reperfusion injury is mediated by leukocytic toll-like receptor-2 and reduced by systemic administration of a novel anti-toll-like receptor-2 antibody. Circulation. 2010;121:80–90.CrossRefPubMed

13.

Mann DL. The emerging role of innate immunity in the heart and vascular system: for whom the cell tolls. Circ Res. 2011;108:133–1145.CrossRef

14.

Rossen RD, Michael LH, Hawkins HK, Youker K, Dreyer WJ, Baughn RE, et al. Cardiolipin-protein complexes and initiation of complement activation after coronary artery occlusion. Circ Res. 1994;75:546–55.CrossRefPubMed

15.

Yanai H, Ban T, Wang Z, Choi MK, Kawamura T, Negishi H, et al. HMGB proteins function as universal sentinels for nucleic-acid-mediated innate immune responses. Nature. 2009;462:99–103. doi:10.1038/nature08512.CrossRefPubMed

16.

Ueno H, Matsuda T, Hashimoto S, Amaya F, Kitamura Y, Tanaka M, et al. Contributions of high mobility group box protein in experimental and clinical acute lung injury. Am J Respir Crit Care Med. 2004;170:1310–6.CrossRefPubMed

17.

Frangogiannis NG. Regulation of the inflammatory response in cardiac repair. Circ Res. 2012;110:159–73. doi:10.1161/CIRCRESAHA.111.243162.CrossRefPubMedCentralPubMed

18.

Frangogiannis NG. The immune system and cardiac repair. Pharmacol Res. 2008;58:88–111. doi:10.1016/j.phrs.2008.06.007.CrossRefPubMedCentralPubMed

19.

Ma XL, Weyrich AS, Lefer DJ, Buerke M, Albertine KH, Kishimoto TK, et al. Monoclonal antibody to L-selectin attenuates neutrophil accumulation and protects ischemic reperfused cat myocardium. Circulation. 1993;88:649–58.CrossRefPubMed

20.

Kubes P, Jutila M, Payne D. Therapeutic potential of inhibiting leukocyte rolling in ischemia/reperfusion. J Clin Invest. 1995;95:2510–9.CrossRefPubMedCentralPubMed

21.

Briaud SA, Ding ZM, Michael LH, Entman ML, Daniel S, Ballantyne CM. Leukocyte trafficking and myocardial reperfusion injury in ICAM-1/P-selectin-knockout mice. Am J Physiol Heart Circ Physiol. 2001;280:H60–7.PubMed

22.

Faxon DP, Gibbons RJ, Chronos NA, Gurbel PA, Sheehan F, HALT-MI Investigators. The effect of blockade of the CD11/CD18 integrin receptor on infarct size in patients with acute myocardial infarction treated with direct angioplasty: the results of the HALT-MI study. J Am Coll Cardiol. 2002;40:1199–204.CrossRefPubMed

23.

Perez RG, Arai M, Richardson C, DiPaula A, Siu C, Matsumoto N, et al. Factors modifying protective effect of anti-CD18 antibodies on myocardial reperfusion injury in dogs. Am J Physiol. 1996;270(1 Pt 2):H53–64.PubMed

24.

Ciz M, Denev P, Kratchanova M, Vasicek O, Ambrozova G, Lojek A. Flavonoids inhibit the respiratory burst of neutrophils in mammals. Oxidative Med Cell Longev. 2012;2012:181295. doi:10.1155/2012/181295.CrossRef

25.

Amulic B, Cazalet C, Hayes GL, Metzler KD, Zychlinsky A. Neutrophil function: from mechanisms to disease. Annu Rev Immunol. 2012;30:459–89. doi:10.1146/annurev-immunol-020711-074942.CrossRefPubMed

26.

Qin F, Simeone M, Patel R. Inhibition of NADPH oxidase reduces myocardial oxidative stress and apoptosis and improves cardiac function in heart failure after myocardial infarction. Free Radic Biol Med. 2007;43:271–81.CrossRefPubMed

27.

Zhao W, Zhao T, Chen Y, Ahokas RA, Sun Y. Reactive oxygen species promote angiogenesis in the infarcted rat heart. Int J Exp Pathol. 2009;90:621–9. doi:10.1111/j.1365-2613.2009.00682.x.CrossRefPubMedCentralPubMed

28.

Mocatta TJ, Pilbrow AP, Cameron VA, Senthilmohan R, Frampton CM, Richards AM, et al. Plasma concentrations of myeloperoxidase predict mortality after myocardial infarction. J Am Coll Cardiol. 2007;49:1993–2000.CrossRefPubMed

29.

Afshar-Kharghan V, Thiagarajan P. Leukocyte adhesion and thrombosis. Curr Opin Hematol. 2006;13:34–9.CrossRefPubMed

30.

Ng LL, Khan SQ, Narayan H, Quinn P, Squire IB, Davies JE. Proteinase 3 and prognosis of patients with acute myocardial infarction. Clin Sci (Lond). 2011;120:231–8. doi:10.1042/CS20100366.

31.

van den Borne SW, Cleutjens JP, Hanemaaijer R, Creemers EE, Smits JF, Daemen MJ, et al. Increased matrix metalloproteinase-8 and −9 activity in patients with infarct rupture after myocardial infarction. Cardiovasc Pathol. 2009;18:37–43. doi:10.1016/j.carpath.2007.12.012.CrossRefPubMed

32.

Ducharme A, Frantz S, Aikawa M, Rabkin E, Lindsey M, Rohde LE, et al. Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction. J Clin Invest. 2000;106:55–62.CrossRefPubMedCentralPubMed

33.

Lindsey ML, Escobar GP, Dobrucki LW, Goshorn DK, Bouges S, Mingoia JT, et al. Matrix metalloproteinase-9 gene deletion facilitates angiogenesis after myocardial infarction. Am J Physiol Heart Circ Physiol. 2006;290:H232–9.CrossRefPubMed

34.

Zamilpa R, Ibarra J, de Castro Brás LE, Ramirez TA, Nguyen N, Halade GV, et al. Transgenic overexpression of matrix metalloproteinase-9 in macrophages attenuates the inflammatory response and improves left ventricular function post-myocardial infarction. J Mol Cell Cardiol. 2012;53:599–608. doi:10.1016/j.yjmcc.2012.07.017.CrossRefPubMedCentralPubMed

35.

Moldovan NI, Goldschmidt-Clermont PJ, Parker-Thornburg J, Shapiro SD, Kolattukudy PE. Contribution of monocytes/macrophages to compensatory neovascularization: the drilling of metalloelastase-positive tunnels in ischemic myocardium. Circ Res. 2000;87:378–84.CrossRefPubMed

36.

Cooper PR, Palmer LJ, Chapple IL. Neutrophil extracellular traps as a new paradigm in innate immunity: friend or foe? Periodontol. 2013;63:165–97. doi:10.1111/prd.12025.CrossRef

37.

de Boer OJ, Li X, Teeling P, Mackaay C, Ploegmakers HJ, van der Loos CM, et al. Neutrophils, neutrophil extracellular traps and interleukin-17 associate with the organisation of thrombi in acute myocardial infarction. Thromb Haemost. 2013;109:290–7. doi:10.1160/TH12-06-0425.CrossRefPubMed

38.

Savchenko AS, Borissoff JI, Martinod K, De Meyer SF, Gallant M, Erpenbeck L, et al. VWF-mediated leukocyte recruitment with chromatin decondensation by PAD4 increases myocardial ischemia/reperfusion injury in mice. Blood. 2014;123:141–8. doi:10.1182/blood-2013-07-514992.CrossRefPubMedCentralPubMed

39.

Maugeri N, Campana L, Gavina M, Covino C, De Metrio M, Panciroli C, et al. Activated platelets present high mobility group box 1 to neutrophils, inducing autophagy and promoting the extrusion of neutrophil extracellular traps. J Thromb Haemost. 2014;12:2074–88. doi:10.1111/jth.12710.CrossRefPubMed

40.

Soehnlein O, Lindbom L. Phagocyte partnership during the onset and resolution of inflammation. Nat Rev Immunol. 2010;10:427–39. doi:10.1038/nri2779.CrossRefPubMed

41.

Huang M, Yang D, Xiang M, Wang J. Role of interleukin-6 in regulation of immune responses to remodeling after myocardial infarction. Heart Fail Rev. 2015;20:25–38. doi:10.1007/s10741-014-9431-1.CrossRefPubMed

42.

Stark MA, Huo Y, Burcin TL, Morris MA, Olson TS, Ley K. Phagocytosis of apoptotic neutrophils regulates granulopoiesis via IL-23 and IL-17. Immunity. 2005;22:285–94.CrossRefPubMed

43.

Ley K, Smith E, Stark MA. IL-17A-producing neutrophil-regulatory Tn lymphocytes. Immunol Res. 2006;34:229–42.CrossRefPubMed

44.

Bratton DL, Henson PM. Neutrophil clearance: when the party is over, clean-up begins. Trends Immunol. 2011;32:350–7. doi:10.1016/j.it.2011.04.009.CrossRefPubMedCentralPubMed

45.

Maddox JF, Hachicha M, Takano T, Petasis NA, Fokin VV, Serhan CN. Lipoxin A4 stable analogs are potent mimetics that stimulate human monocytes and THP-1 cells via a G-protein-linked lipoxin A4 receptor. J Biol Chem. 1997;272:6972–8.CrossRefPubMed

46.

Novack V, Pencina M, Zahger D, Fuchs L, Nevzorov R, Jotkowitz A, et al. Routine laboratory results and thirty day and one-year mortality risk following hospitalization with acute decompensated heart failure. PLoS ONE. 2010;5:e12184. doi:10.1371/journal.pone.0012184.CrossRefPubMedCentralPubMed

47.

Cooper HA, Exner DV, Waclawiw MA, Domanski MJ. White blood cell count and mortality in patients with ischemic and nonischemic left ventricular systolic dysfunction (an analysis of the studies of left ventricular dysfunction [SOLVD]). Am J Cardiol. 1999;84:252–7.CrossRefPubMed

48.

Arruda-Olson AM, Reeder GS, Bell MR, Weston SA, Roger VL. Neutrophilia predicts death and heart failure after myocardial infarction: a community-based study. Circ Cardiovasc Qual Outcomes. 2009;2:656–62. doi:10.1161/CIRCOUTCOMES.108.831024.CrossRefPubMedCentralPubMed

49.

Rashidi F, Rashidi A, Golmohamadi A, Hoseinzadeh E, Mohammadi B, Mirzajani H, et al. Does absolute neutrophilia predict early congestive heart failure after acute myocardial infarction? A cross-sectional study. South Med J. 2008;101:19–23. doi:10.1097/SMJ.0b013e31815d3e11.CrossRefPubMed

50.

Uthamalingam S, Patvardhan EA, Subramanian S, Ahmed W, Martin W, Daley M, et al. Utility of the neutrophil to lymphocyte ratio in predicting long-term outcomes in acute decompensated heart failure. Am J Cardiol. 2011;107:433–8. doi:10.1016/j.amjcard.2010.09.039.CrossRefPubMed

51.

Yıldız A, Yüksel M, Oylumlu M, Polat N, Akıl MA, Acet H. The association between the neutrophil/lymphocyte ratio and functional capacity in patients with idiopathic dilated cardiomyopathy. Anadolu Kardiyol Derg. 2014. doi:10.5152/akd.2014.5131.

52.

Avci A, Alizade E, Fidan S, Yesin M, Guler Y, Kargin R, et al. Neutrophil/lymphocyte ratio is related to the severity of idiopathic dilated cardiomyopathy. Scand Cardiovasc J. 2014;48:202–8. doi:10.3109/14017431.2014.932922.CrossRefPubMed

53.

von Haehling S, Schefold JC, Jankowska E, Doehner W, Springer J, Strohschein K, et al. Leukocyte redistribution: effects of beta blockers in patients with chronic heart failure. PLoS One. 2009;4:e6411. doi:10.1371/journal.pone.0006411.CrossRef

54.

Vaduganathan M, Greene SJ, Butler J, Sabbah HN, Shantsila E, Lip GY, et al. The immunological axis in heart failure: importance of the leukocyte differential. Heart Fail Rev. 2013;18:835–45. doi:10.1007/s10741-012-9352-9.CrossRefPubMed

55.

Elenkov IJ, Wilder RL, Chrousos GP, Vizi ES. The sympathetic nerve—an integrative interface between two supersystems: the brain and the immune system. Pharmacol Rev. 2000;52:595–638.PubMed

56.

Singer AJ, Clark RA. Cutaneous wound healing. N Engl J Med. 1999;341:738–46.CrossRefPubMed

57.

Jung K, Kim P, Leuschner F, Gorbatov R, Kim JK, Ueno T, et al. Endoscopic time-lapse imaging of immune cells in infarcted mouse hearts. Circ Res. 2013;112:891–9. doi:10.1161/CIRCRESAHA.111.300484.CrossRefPubMed

58.

Nahrendorf M, Swirski FK, Aikawa E, Stangenberg L, Wurdinger T, Figueiredo JL, et al. The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions. J Exp Med. 2007;204:3037–47.CrossRefPubMedCentralPubMed

59.

Saxena A, Chen W, Su Y, Rai V, Uche OU, Li N, et al. IL-1 induces proinflammatory leukocyte infiltration and regulates fibroblast phenotype in the infarcted myocardium. J Immunol. 2013;191:4838–48. doi:10.4049/jimmunol.1300725.CrossRefPubMed

60.

Nahrendorf M, Swirski FK. Monocyte and macrophage heterogeneity in the heart. Circ Res. 2013;112:1624–33. doi:10.1161/CIRCRESAHA.113.300890.CrossRefPubMedCentralPubMed

61.

van der Laan AM, Ter Horst EN, Delewi R, Begieneman MP, Krijnen PA, Hirsch A, et al. Monocyte subset accumulation in the human heart following acute myocardial infarction and the role of the spleen as monocyte reservoir. Eur Heart J. 2014;35:376–85. doi:10.1093/eurheartj/eht331.CrossRefPubMedCentralPubMed

62.

Dewald O, Zymek P, Winkelmann K, Koerting A, Ren G, Abou-Khamis T, et al. CCL2/monocyte chemoattractant protein-1 regulates inflammatory responses critical to healing myocardial infarcts. Circ Res. 2005;96:881–9.CrossRefPubMed

63.

Lee WW, Marinelli B, van der Laan AM, Sena BF, Gorbatov R, Leuschner F, et al. PET/MRI of inflammation in myocardial infarction. J Am Coll Cardiol. 2012;59:153–63. doi:10.1016/j.jacc.2011.08.066.CrossRefPubMedCentralPubMed

64.

Panizzi P, Swirski FK, Figueiredo JL, Waterman P, Sosnovik DE, Aikawa E, et al. Impaired infarct healing in atherosclerotic mice with Ly-6C^hi monocytosis. J Am Coll Cardiol. 2010;55:1629–38. doi:10.1016/j.jacc.2009.08.089.CrossRefPubMedCentralPubMed

65.

Majmudar MD, Keliher EJ, Heidt T, Leuschner F, Truelove J, Sena BF, et al. Monocyte-directed RNAi targeting CCR2 improves infarct healing in atherosclerosis-prone mice. Circulation. 2013;127:2038–46. doi:10.1161/CIRCULATIONAHA.112.000116.CrossRefPubMedCentralPubMed

66.

Tsujioka H, Imanishi T, Ikejima H, Kuroi A, Takarada S, Tanimoto T, et al. Impact of heterogeneity of human peripheral blood monocyte subsets on myocardial salvage in patients with primary acute myocardial infarction. J Am Coll Cardiol. 2009;54:130–8. doi:10.1016/j.jacc.2009.04.021.CrossRefPubMed

67.

Frantz S, Hofmann U, Fraccarollo D, Schäfer A, Kranepuhl S, Hagedorn I, et al. Monocytes/macrophages prevent healing defects and left ventricular thrombus formation after myocardial infarction. FASEB J. 2013;27:871–81. doi:10.1096/fj.12-214049.CrossRefPubMed

68.•

Courties G, Heidt T, Sebas M, Iwamoto Y, Jeon D, Truelove J, et al. In vivo silencing of the transcription factor IRF5 reprograms the macrophage phenotype and improves infarct healing. J Am Coll Cardiol. 2014;63:1556–66. doi:10.1016/j.jacc.2013.11.023. siRNA was used to silence IRF5 in macrophages and successfully manipulated polarization towards a M2 phenotype attenuating post MI remodeling.CrossRefPubMedCentralPubMed

69.

Weirather J, Hofmann UD, Beyersdorf N, Ramos GC, Vogel B, Frey A, et al. Foxp3+ CD4+ T cells improve healing after myocardial infarction by modulating monocyte/macrophage differentiation. Circ Res. 2014;115:55–67. doi:10.1161/CIRCRESAHA.115.303895.CrossRefPubMed

70.

Maekawa Y, Anzai T, Yoshikawa T, Asakura Y, Takahashi T, Ishikawa S, et al. Prognostic significance of peripheral monocytosis after reperfused acute myocardial infarction: a possible role for left ventricular remodeling. J Am Coll Cardiol. 2002;39:241–6.CrossRefPubMed

71.

Nahrendorf M, Pittet MJ, Swirski FK. Monocytes: protagonists of infarct inflammation and repair after myocardial infarction. Circulation. 2010;121:2437–45. doi:10.1161/CIRCULATIONAHA.109.916346.CrossRefPubMedCentralPubMed

72.

Swirski FK, Nahrendorf M, Etzrodt M, Wildgruber M, Cortez-Retamozo V, Panizzi P, et al. Identification of splenic reservoir monocytes and their deployment to inflammatory sites. Science. 2009;325:612–6. doi:10.1126/science.1175202.CrossRefPubMedCentralPubMed

73.

Leuschner F, Panizzi P, Chico-Calero I, Lee WW, Ueno T, Cortez-Retamozo V, et al. Angiotensin-converting enzyme inhibition prevents the release of monocytes from their splenic reservoir in mice with myocardial infarction. Circ Res. 2010;107:1364–73. doi:10.1161/CIRCRESAHA.110.227454.CrossRefPubMedCentralPubMed

74.

Leuschner F, Rauch PJ, Ueno T, Gorbatov R, Marinelli B, Lee WW, et al. Rapid monocyte kinetics in acute myocardial infarction are sustained by extramedullary monocytopoiesis. J Exp Med. 2012;209:123–37. doi:10.1084/jem.20111009.CrossRefPubMedCentralPubMed

75.

Dutta P, Courties G, Wei Y, Leuschner F, Gorbatov R, Robbins CS, et al. Myocardial infarction accelerates atherosclerosis. Nature. 2012;487:325–9. doi:10.1038/nature11260.CrossRefPubMedCentralPubMed

76.•

Ismahil MA, Hamid T, Bansal SS, Patel B, Kingery JR, Prabhu SD. Remodeling of the mononuclear phagocyte network underlies chronic inflammation and disease progression in heart failure: critical importance of the cardiosplenic axis. Circ Res. 2014;114:266–82. doi:10.1161/CIRCRESAHA.113.301720. This is the first article to demonstrate that the spleen regulates both chronic inflammation and the progression of pathological LV remodeling.CrossRefPubMed

77.

Alam SR, Shah AS, Richards J, Lang NN, Barnes G, Joshi N, et al. Ultrasmall superparamagnetic particles of iron oxide in patients with acute myocardial infarction: early clinical experience. Circ Cardiovasc Imaging. 2012;5:559–65.CrossRefPubMed

78.

Yilmaz A, Dengler MA, van der Kuip H, Yildiz H, Rösch S, Klumpp S, et al. Imaging of myocardial infarction using ultrasmall superparamagnetic iron oxide nanoparticles: a human study using a multi-parametric cardiovascular magnetic resonance imaging approach. Eur Heart J. 2013;34:462–75. doi:10.1093/eurheartj/ehs366.CrossRefPubMed

Titel: Cellular Immunity and Cardiac Remodeling After Myocardial Infarction: Role of Neutrophils, Monocytes, and Macrophages
verfasst von: Hisahito Shinagawa
Stefan Frantz
Publikationsdatum: 01.06.2015
Verlag: Springer US
Erschienen in: Current Heart Failure Reports / Ausgabe 3/2015
Print ISSN: 1546-9530
Elektronische ISSN: 1546-9549
DOI: https://doi.org/10.1007/s11897-015-0255-7

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