Mechanisms of leukocyte recruitment to atherosclerotic lesions: Future prospects

Current Opinion in Lipidology

Volumn 15, Issue 5, 2004, Pages 553-558

  Eriksson, Einar E ^a  

^a KAROLINSKA INSTITUTE   (Sweden)

Author keywords

Atherosclerosis; Cell adhesion molecules; Chemokines; Endothelium; Leukocyte

Indexed keywords

1 [3 (4 BIPHENYLYLMETHYL) 4 HYDROXYCHROMAN 7 YL]CYCLOPENTANECARBOXYLIC ACID; APOLIPOPROTEIN E; ARACHIDONATE 5 LIPOXYGENASE; CELL ADHESION MOLECULE; CHEMOATTRACTANT; CHEMOKINE; CHEMOKINE RECEPTOR CXCR3; ENDOTHELIAL LEUKOCYTE ADHESION MOLECULE 1; LEUKOTRIENE B4; LEUKOTRIENE B4 RECEPTOR; PADGEM PROTEIN; RANTES; SELECTIN ANTAGONIST; THROMBOCYTE FACTOR 4;

ATHEROSCLEROSIS; CELL FUNCTION; CELL INVASION; CELL TYPE; ENDOTHELIUM CELL; EXPERIMENTAL MODEL; HUMAN; HYPERPLASIA; LEUKOCYTE; LEUKOCYTE ADHERENCE; LEUKOCYTE MIGRATION; MONOCYTE; NONHUMAN; PRIORITY JOURNAL; PROTECTION; PROTEIN SECRETION; PROTEIN TARGETING; RECEPTOR BLOCKING; REVIEW; SIGNAL TRANSDUCTION; THROMBOCYTE ADHESION; THROMBOCYTE FUNCTION;

ANIMALS; ARACHIDONATE 5-LIPOXYGENASE; ARTERIOSCLEROSIS; CELL ADHESION; CHEMOKINES; CHEMOKINES, CC; HUMANS; LEUKOCYTES; MEMBRANE PROTEINS; PLATELET ADHESIVENESS; PLATELET FACTOR 4; RANTES; RECEPTORS, CHEMOKINE; RECEPTORS, LEUKOTRIENE B4; RECEPTORS, PURINERGIC P2; SIGNAL TRANSDUCTION;

EID: 5044232471     PISSN: 09579672     EISSN: None     Source Type: Journal    
DOI: 10.1097/00041433-200410000-00009     Document Type: Review

References (52)

1. Crisby M, Nordin-Fredriksson G, Shah PK, et al. Pravastatin treatment increases collagen content and decreases lipid content, inflammation, metalloproteinases, and cell death in human carotid plaques: implications for plaque stabilization. Circulation 2001; 103:926-933.
2. Springer TA. Traffic signals for lymphocyte recirculation and leukocyte emigration: the multistep paradigm. Cell 1994; 76:301-314.
3. Ulbrich H, Eriksson EE, Lindbom L. Leukocyte and endothelial cell adhesion molecules as targets for therapeutic interventions in inflammatory disease. Trends Pharmacol Sci 2003; 24:640-647. A recent review on the potential for blockage of CAMs as treatment for inflammatory disease.
4. Eriksson EE. Leukocyte recruitment to atherosclerotic lesions, a complex web of dynamic cellular and molecular interactions. Curr Drug Targets Cardiovasc Haematol Disord 2003; 3:309-325. A recent and comprehensive review of the current knowledge of the mechanisms that recruit leukocytes to atherosclerotic lesions.
5. Dong ZM, Chapman SM, Brown AA, et al. The combined role of P- and E-selectins in atherosclerosis. J Clin Invest 1998; 102:145-152.
6. Frenette PS, Mayadas TN, Rayburn H, et al. Susceptibility to infection and altered hematopoiesis in mice deficient in both P- and E-selectins. Cell 1996; 84:563-574.
7. Nageh MF, Sandberg ET, Marotti KR, et al. Deficiency of inflammatory cell adhesion molecules protects against atherosclerosis in mice. Arterioscler Thromb Vasc Biol 1997; 17:1517-1520.
8. Yoshida M, Takano Y, Sasaoka T, et al. E-selectin polymorphism associated with myocardial infarction causes enhanced leukocyte-endotnelial interactions under flow conditions. Arterioscler Thromb Vasc Biol 2003; 23:783-788. This paper shows that the Ser128Arg polymorphism in human E-selectin is associated with MI as well as the enhanced adhesive capacity of this molecule under flow conditions.
9. Burger PC, Wagner DD. Platelet P-selectin facilitates atherosclerotic lesion development. Blood 2003; 101:2661-2666. This paper uses bone marrow transfer in mice to determine the respective effects of platelet and endothelial P-selectin in the development of atherosclerosis.
10. Massberg S, Brand K, Gruner S, et al. A critical role of platelet adhesion in the initiation of atherosclerotic lesion formation. J Exp Med 2002; 196:887-896.
11. Huo Y, Schober A, Forlow SB, et al. Circulating activated platelets exacerbate atherosclerosis in mice deficient in apolipoprotein E. Nat Med 2003; 9:61-67. This paper demonstrates that platelets interact with atherosclerotic endothelium in vivo, and that these cells deposit chemokines (PF4, RANTES) on the endothelial surface. These chemokines subsequently increase the recruitment of leukocytes to atherosclerotic plaque.
12. da Costa Martins P, van den Berk N, Ulfman LH, et al. Platelet-monocyte complexes support monocyte adhesion to endothelium by enhancing secondary tethering and cluster formation. Arterioscler Thromb Vasc Biol 2004; 24:193-199. A well-performed study that shows the potential for platelets to bind to monocytes and mediate initial tethering between platelet-monocyte clusters and endothelial cells.
13. Kalvegren H, Majeed M, Bengtsson T. Chlamydia pneumoniae binds to platelets and triggers P-selectin expression and aggregation: a causal role in cardiovascular disease? Arterioscler Thromb Vasc Biol 2003; 23:1677-1683. This study demonstrates that C. pneumoniae binds to platelets and induces the activation and expression of P-selectin on the platelet surface. The blockage of glycoprotein IIb/IIIa decreases this effect.
14. -/- mice.
15. Manka D, Forlow SB, Sanders JM, et al. Critical role of platelet P-selectin in the response to arterial injury in apolipoprotein-E-deficient mice. Arterioscler Thromb Vasc Biol 2004; in press.
16. Ortlepp JR, Vesper K, Mevissen V, et al. Chemokine receptor (CCR2) genotype is associated with myocardial infarction and heart failure in patients under 65 years of age. J Mol Med 2003; 81:363-367. A careful study that demonstrates associations between the CCR2 V641 polymorphism, MI and reduced left ventricular function.
17. Petrkova J, Cermakova Z, Drabek J, et al. CC chemokine receptor (CCR)2 polymorphism in Czech patients with myocardial infarction. Immunol Lett 2003; 88:53-55. A study with a relatively small amount of material that shows a relationship between the CCR2 V64I polymorphism and MI in women but not in men.
18. Gonzalez P, Alvarez R, Batalla A, et al. Genetic variation at the chemokine receptors CCR5/CCR2 in myocardial infarction. Genes Immun 2001; 2:191-195.
19. Szalai C, Duba J, Prohaszka Z, et al. Involvement of polymorphisms in the chemokine system in the susceptibility for coronary artery disease (CAD). Coincidence of elevated Lp(a) and MCP-1-2518 G/G genotype in CAD patients. Atherosclerosis 2001; 158:233-239.
20. Boisvert WA, Santiago R, Curtiss LK, Terkeltaub RA. A leukocyte homologue of the IL-8 receptor CXCR-2 mediates the accumulation of macrophages in atherosclerotic lesions of LDL receptor-deficient mice. J Clin Invest 1998; 101:353-363.
21. -/- mice.
22. Veillard NR, Kwak B, Pelli G, et al. Antagonism of RANTES receptors reduces atherosclerotic plaque formation in mice. Circ Res 2004; 94:253-261. This study demonstrates that the blockage of RANTES signaling protects against atherosclerosis, and thus implicates RANTES receptors as potential drug targets.
23. -/- mice. Effects were evident also in mice heterozygous for the targeted allele.
24. -/- mice, and that fractalkine is expressed predominantly in smooth muscle cells in lesions.
25. McDermott DH, Halcox JP, Schenke WH, et al. Association between polymorphism in the chemokine receptor CX3CR1 and coronary vascular endothelial dysfunction and atherosclerosis. Circ Res 2001; 89:401-407.
26. Ghilardi G, Biondi ML, Turri O, et al. Internal carotid artery occlusive disease and polymorphisms of fractalkine receptor CX3CR1: a genetic risk factor. Stroke 2004; in press.
27. Schafer A, Schulz C, Eigenthaler M, et al. Novel role of the membrane-bound chemokine fractalkine in platelet activation and adhesion. Blood 2004; 103:407-412. A well-performed in-vitro study that demonstrates the potential for fractalkine to induce the activation of platelets and the expression of P-selectin on the platelet surface.
28. Lucas AD, Bursill C, Guzik TJ, et al. Smooth muscle cells in human atherosclerotic plaques express the fractalkine receptor CX3CR1 and undergo chemotaxis to the CX3C chemokine fractalkine (CX3CL1). Circulation 2003; 108:2498-2504. A study performed mainly by immunohistochemical techniques that demonstrates the expression of CX3CR1 in several cell types in lesions including smooth muscle cells.
29. Ahn SY, Cho CH, Park KG, et al. Tumor necrosis factor-alpha induces fractalkine expression preferentially in arterial endothelial cells and mithramycin A suppresses TNF-alpha-induced fractalkine expression. Am J Pathol 2004; 164:1663-1672. In-vivo and in-vitro data demonstrating that fractalkine is expressed in endothelial cells after stimulation with TNF-α. Expression was reduced by inhibitors of nuclear factor kappa B-mediated transcription.
30. Ollivier V, Faure S, Tarantino N, et al. Fractalkine/CX3CL1 production by human aortic smooth muscle cells impairs monocyte procoagulant and inflammatory responses. Cytokine 2003; 21:303-311. This study shows that smooth muscle cells express fractalkine in response to lipopolysaccharide and that monocytes adhere to activated smooth muscle cells by interactions with CX3CR1. The release of TNF-α and tissue factor from monocytes was attenuated when cells adhered to lipopolysaccharide and fractalkine compared with when cells adhered to lipopolysaccharide alone.
31. -/- mice was attenuated in mice deficient in the BLT1 receptor at early stages (4 and 8 weeks after the onset of western diet). However, in later stages (19 weeks) no protective effect was seen.
32. Aiello RJ, Bourassa PA, Lindsey S, et al. Leukotriene B4 receptor antagonism reduces monocytic foam cells in mice. Arterioscler Thromb Vasc Biol 2002; 22:443-449.
33. Spanbroek R, Grabner R, Lotzer K, et al. Expanding expression of the 5-lipoxygenase pathway within the arterial wall during human atherogenesis. Proc Natl Acad Sci USA 2003; 100:1238-1243. This study shows that the expression of 5-lipoxygenase is abundant in atherosclerotic lesions and that many cell types including macrophages, dendritic cells and granulocytes are responsible for the high activity of this enzyme in plaque.
34. Pitsilos S, Hunt J, Mohler ER, et al. Platelet factor 4 localization in carotid atherosclerotic plaques: correlation with clinical parameters. Thromb Haemost 2003; 90:1112-1120. The study shows the presence of PF4 in endothelial cells and in macrophages of human lesions. NAP-2 was detected in advanced lesions but not at early stages.
35. Wuttge DM, Zhou X, Sheikine Y, et al. CXCL16/SR-PSOX is an interferon-gamma-regulated chemokine and scavenger receptor expressed in atherosclerotic lesions. Arterioscler Thromb Vasc Biol 2004; 24:750-755. This study demonstrates the expression of CXCL16 in macrophages and T lymphocytes in plaque.
36. -/- mice.
37. Murphy N, Bruckdorfer KR, Grimsditch DC, et al. Temporal relationships between circulating levels of CC and CXC chemokines and developing atherosclerosis in apolipoprotein E*3 Leiden mice. Arterioscler Thromb Vasc Biol 2003; 23:1615-1620. The study shows that serum chemokine levels are closely linked to the intake of fatty diet and serum cholesterol levels.
38. Holven KB, Myhre AM, Aukrust P, et al. Patients with familial hypercholesterolaemia show enhanced spontaneous chemokine release from peripheral blood mononuclear cells ex vivo. Dependency of xanthomas/xanthelasms, smoking and gender. Eur Heart J 2003; 24:1756-1762. A study that shows that peripheral blood mononuclear cells from patients with familial hypercholesterolemia release increased amounts of MIP-1α, MIP-1β and IL-8 and that the release is enhanced in women, in cigarette smokers and in patients with xantelasms.
39. Kao J, Kobashigawa J, Fishbein MC, et al. Elevated serum levels of the CXCR3 chemokine ITAC are associated with the development of transplant coronary artery disease. Circulation 2003; 107:1958-1961. This study shows the expression of ITAC on the endothelium of transplant arteries and the association between ITAC expression and the presence of transmigrated monocytes expressing CXCR3.
40. Mach F, Sauty A, Iarossi AS, et al. Differential expression of three T lymphocyte-activating CXC chemokines by human atheroma-associated cells. J Clin Invest 1999; 104:1041-1050.
41. Eriksson EE, Werr J, Guo Y, et al. Direct observations in vivo on the role of endothelial selectins and alpha(4) integrin in cytokine-induced leukocyte-endothelium interactions in the mouse aorta. Circ Res 2000; 86:526-533.
42. Eriksson EE, Xie X, Werr J, et al. Direct viewing of atherosclerosis in vivo: plaque invasion by leukocytes is initiated by the endothelial selectins. FASEB J 2001; 15:1149-1157.
43. Ramos CL, Huo Y, Jung U, et al. Direct demonstration of P-selectin- and VCAM-1-dependent mononuclear cell rolling in early atherosclerotic lesions of apolipoprotein E-deficient mice. Circ Res 1999; 84:1237-1244.
44. -/- mice.
45. de Boer OJ, van der Wal AC, Teeling P, Becker AE. Leucocyte recruitment in rupture prone regions of lipid-rich plaques: a prominent role for neovascularization? Cardiovasc Res 1999; 41:443-449.
46. Lusis AJ. Atherosclerosis. Nature 2000; 407:233-241.
47. Robertson AK, Rudling M, Zhou X, et al. Disruption of TGF-beta signaling in T cells accelerates atherosclerosis. J Clin Invest 2003; 112:1342-1350. A proatherogenic role for T lymphocytes is convincingly shown by the enhanced formation of lesions in mice in which signaling through transforming growth factor beta in T cells is disrupted by the introduction of a dominant negative transforming growth factor beta receptor II.
48. Caligiuri G, Nicoletti A, Poirier B, Hansson GK. Protective immunity against atherosclerosis carried by B cells of hypercholesterolemic mice. J Clin Invest 2002; 109:745-753.
49. Mallat Z, Gojova A, Brun V, et al. Induction of a regulatory T cell type 1 response reduces the development of atherosclerosis in apolipoprotein E-knockoul mice. Circulation 2003; 108:1232-1237. The potential role for regulatory T cells in atherosclerosis is demonstrated in this study. Ovalbumin-activated regulatory cells were transferred to atherosclerotic mice challenged with this antigen. Mice that received regulatory cells were protected from atherosclerosis.
50. Laine P, Kaartinen M, Penttila A, et al. Association between myocardial infarction and the mast cells in the adventitia of the infarct-related coronary artery. Circulation 1999; 99:361-369.
51. -/- mice, indicating that lipid antigens acting through natural killer T cells may be of importance in the disease. Moreover, the activation of endogenous natural killer T cells by treatment with αGalCer caused increased development of atherosclerosis, suggesting that soluble mediators secreted by natural killer T cells promote atherogenesis.
52. Naruko T, Ueda M, Haze K, et al. Neutrophil infiltration of culprit lesions in acute coronary syndromes. Circulation 2002; 106:2894-2900.