全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...
PLOS ONE  2007 

Neutrophil Activation Status in Stable Coronary Artery Disease

DOI: 10.1371/journal.pone.0001056

Full-Text   Cite this paper   Add to My Lib

Abstract:

Background During the last years, neutrophils have emerged as important players in atherogenesis. They are highly activated in peripheral blood of patients with unstable angina. Moreover, a primed state of circulating neutrophils has been proposed in patients with stable angina. Our aim was to investigate the neutrophil activation status in patients with stable coronary artery disease (CAD) at conventional drug treatment. Methodology and Principal Findings Thirty patients with stable CAD and 30 healthy controls were included using a paired design. The neutrophil expression of CD18 and high-affinity state of CD11b was analysed by flow cytometry before and after stimulation with chemoattractants. Also, the production of reactive oxygen species (ROS) was determined by chemiluminescence. During basal conditions, the neutrophil expression of CD18 or high-affinity state of CD11b did not differ between patients and controls. Chemoattractants (Interleukin-8 and Leukotriene B4) did not increase either the expression or the amount of high-affinity CD11b/CD18-integrins in CAD patients compared to controls, and had no effect on the production of ROS. On the other hand, the ROS production in response to C3bi-opsonised yeast particles and the neutrophils' inherent capacity to produce ROS were both significantly decreased in patients. Conclusion/Significance We could not find any evidence that neutrophils in patients with stable CAD were primed, i.e. more prone to activation, compared to cells from healthy controls. According to our data, the circulating neutrophils in CAD patients rather showed an impaired activation status. It remains to be elucidated whether the neutrophil dysfunction in CAD is mainly a marker of chronic disease, an atherogenic factor or a consequence of the drug treatment.

References

[1]  Ott I, Neumann FJ, Gawaz M, Schmitt M, Schomig A (1996) Increased neutrophil-platelet adhesion in patients with unstable angina. Circulation 94: 1239–1246.
[2]  Buffon A, Biasucci LM, Liuzzo G, D'Onofrio G, Crea F, et al. (2002) Widespread coronary inflammation in unstable angina. N Engl J Med 347: 5–12.
[3]  Patel PB, Pfau SE, Cleman MW, Brennan JJ, Howes C, et al. (2004) Comparison of coronary artery specific leukocyte-platelet conjugate formation in unstable versus stable angina pectoris. Am J Cardiol 93: 410–413.
[4]  Naruko T, Ueda M, Haze K, van der Wal AC, van der Loos CM, et al. (2002) Neutrophil infiltration of culprit lesions in acute coronary syndromes. Circulation 106: 2894–2900.
[5]  Madjid M, Awan I, Willerson JT, Casscells SW (2004) Leukocyte count and coronary heart disease: implications for risk assessment. J Am Coll Cardiol 44: 1945–1956.
[6]  Mehta J, Dinerman J, Mehta P, Saldeen TG, Lawson D, et al. (1989) Neutrophil function in ischemic heart disease. Circulation 79: 549–556.
[7]  Lindmark E, Wallentin L, Siegbahn A (2001) Blood cell activation, coagulation, and inflammation in men and women with coronary artery disease. Thromb Res 103: 249–259.
[8]  Egger G, Burda A, Obernosterer A, Mitterhammer H, Kager G, et al. (2001) Blood polymorphonuclear leukocyte activation in atherosclerosis: effects of aspirin. Inflammation 25: 129–135.
[9]  Guasti L, Marino F, Cosentino M, Cimpanelli M, Maio RC, et al. (2006) Simvastatin treatment modifies polymorphonuclear leukocyte function in high-risk individuals: a longitudinal study. J Hypertens 24: 2423–2430.
[10]  Paulsson J, Dadfar E, Held C, Jacobson SH, Lundahl J (2007) Activation of peripheral and in vivo transmigrated neutrophils in patients with stable coronary artery disease. Atherosclerosis 192: 328–334.
[11]  Nijm J, Wikby A, Tompa A, Olsson AG, Jonasson L (2005) Circulating levels of proinflammatory cytokines and neutrophil-platelet aggregates in patients with coronary artery disease. Am J Cardiol 95: 452–456.
[12]  Price DT, Loscalzo J (1999) Cellular adhesion molecules and atherogenesis. Am J Med 107: 85–97.
[13]  Hansson GK (2005) Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med 352: 1685–1695.
[14]  Springer TA (1990) Adhesion receptors of the immune system. Nature 346: 425–434.
[15]  Gahmberg CG, Fagerholm S (2002) Activation of leukocyte beta2-integrins. Vox Sang 83 Suppl 1: 355–358.
[16]  Carman CV, Springer TA (2003) Integrin avidity regulation: are changes in affinity and conformation underemphasized? Curr Opin Cell Biol 15: 547–556.
[17]  Diamond MS, Garcia-Aguilar J, Bickford JK, Corbi AL, Springer TA (1993) The I domain is a major recognition site on the leukocyte integrin Mac-1 (CD11b/CD18) for four distinct adhesion ligands. J Cell Biol 120: 1031–1043.
[18]  Lundqvist H, Dahlgren C (1995) The serine protease inhibitor diisopropylfluorophosphate inhibits neutrophil NADPH-oxidase activity induced by the calcium ionophore ionomycin and serum opsonised yeast particles. Inflamm Res 44: 510–517.
[19]  Kim M, Carman CV, Yang W, Salas A, Springer TA (2004) The primacy of affinity over clustering in regulation of adhesiveness of the integrin {alpha}L{beta}2. J Cell Biol 167: 1241–1253.
[20]  Rothenbacher D, Muller-Scholze S, Herder C, Koenig W, Kolb H (2006) Differential expression of chemokines, risk of stable coronary heart disease, and correlation with established cardiovascular risk markers. Arterioscler Thromb Vasc Biol 26: 194–199.
[21]  Boekholdt SM, Peters RJ, Hack CE, Day NE, Luben R, et al. (2004) IL-8 plasma concentrations and the risk of future coronary artery disease in apparently healthy men and women: the EPIC-Norfolk prospective population study. Arterioscler Thromb Vasc Biol 24: 1503–1508.
[22]  Ali H, Richardson RM, Haribabu B, Snyderman R (1999) Chemoattractant receptor cross-desensitization. J Biol Chem 274: 6027–6030.
[23]  Sarndahl E, Bokoch GM, Boulay F, Stendahl O, Andersson T (1996) Direct or C5a-induced activation of heterotrimeric Gi2 proteins in human neutrophils is associated with interaction between formyl peptide receptors and the cytoskeleton. J Biol Chem 271: 15267–15271.
[24]  Heit B, Tavener S, Raharjo E, Kubes P (2002) An intracellular signaling hierarchy determines direction of migration in opposing chemotactic gradients. J Cell Biol 159: 91–102.
[25]  Beller DI, Springer TA, Schreiber RD (1982) Anti-Mac-1 selectively inhibits the mouse and human type three complement receptor. J Exp Med 156: 1000–1009.
[26]  Cougoule C, Wiedemann A, Lim J, Caron E (2004) Phagocytosis, an alternative model system for the study of cell adhesion. Semin Cell Dev Biol 15: 679–689.
[27]  Prasad K (2006) C-reactive protein (CRP)-lowering agents. Cardiovasc Drug Rev 24: 33–50.
[28]  Greenwood J, Steinman L, Zamvil SS (2006) Statin therapy and autoimmune disease: from protein prenylation to immunomodulation. Nat Rev Immunol 6: 358–370.
[29]  Yang YY, Hu CJ, Chang SM, Tai TY, Leu SJ (2004) Aspirin inhibits monocyte chemoattractant protein-1 and interleukin-8 expression in TNF-alpha stimulated human umbilical vein endothelial cells. Atherosclerosis 174: 207–213.
[30]  Papayianni A, Serhan CN, Brady HR (1996) Lipoxin A4 and B4 inhibit leukotriene-stimulated interactions of human neutrophils and endothelial cells. J Immunol 156: 2264–2272.
[31]  Patcha V, Wigren J, Winberg ME, Rasmusson B, Li J, et al. (2004) Differential inside-out activation of beta2-integrins by leukotriene B4 and fMLP in human neutrophils. Exp Cell Res 300: 308–319.
[32]  Fiorucci S, Distrutti E, Mencarelli A, Morelli A, Laufor SA, et al. (2003) Evidence that 5-lipoxygenase and acetylated cyclooxygenase 2-derived eicosanoids regulate leukocyte-endothelial adherence in response to aspirin. Br J Pharmacol 139: 1351–1359.
[33]  Diamond MS, Springer TA (1993) A subpopulation of Mac-1 (CD11b/CD18) molecules mediates neutrophil adhesion to ICAM-1 and fibrinogen. J Cell Biol 120: 545–556.
[34]  Hed J, Stendahl O (1982) Differences in the ingestion mechanisms of IgG and C3b particles in phagocytosis by neutrophils. Immunology 45: 727–736.
[35]  Wilsson A, Lundqvist H, Gustafsson M, Stendahl O (1996) Killing of phagocytosed Staphylococcus aureus by human neutrophils requires intracellular free calcium. J Leukoc Biol 59: 902–907.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133