Detection of circulating platelet-monocyte complexes in persons infected with human immunodeficiency virus type-1

被引:47
作者
Singh, Meera V. [1 ]
Davidson, Donna C. [1 ]
Kiebala, Michelle [1 ]
Maggirwar, Sanjay B. [1 ]
机构
[1] Univ Rochester, Med Ctr, Dept Microbiol & Immunol, Rochester, NY 14642 USA
关键词
Platelet-monocyte complexes; HIV-1; CD16+monocytes; Whole blood; Flow cytometry; LEUKOCYTE INTERACTION; HIV-INFECTION; P-SELECTIN; ACTIVATION; DEMENTIA; ADHESION; SUBSET; BLOOD; AIDS;
D O I
10.1016/j.jviromet.2012.02.005
中图分类号
Q5 [生物化学];
学科分类号
071010 ; 081704 ;
摘要
Activated platelets form transient aggregates with monocytes in circulation and have a half-life of approximately 30-60 min. These complexes are increased in various inflammatory conditions and are an early marker of myocardial infarction. HIV-1 infection is associated with chronic inflammation, and increased CD16(+) inflammatory monocytes have been observed in these individuals, probably as a result of increased interaction with platelets. However, narrow detection period and platelet activation during sample processing pose significant problems in detecting platelet-monocyte complexes (PMCs). A method was standardized addressing these difficulties, to enumerate PMCs involving CD16(+) or CD16(-) monocytes in whole blood using flow cytometry. Blood collected from healthy individuals was treated with either collagen (for platelet activation) or LPS (for monocyte activation) and subsequently used to study effect of these treatments on PMC formation. This method was also validated for the ex vivo quantitation of PMCs in blood obtained from persons infected with HIV. The in vitro results demonstrated that platelet activation, but not monocyte activation, resulted in significant increase in PMC formation. There was a significant increase in CD16(+) PMCs and platelet activation, in samples obtained from persons infected with HIV as compared to those without HIV infection. Furthermore, PMC percentages correlated positively with platelet activation. These findings improve the ability to detect PMCs and shed light on HIV pathogenesis. (C) 2012 Elsevier B.V. All rights reserved.
引用
收藏
页码:170 / 176
页数:7
相关论文
共 25 条
[1]   Cutting edge: Inflammatory responses can be triggered by TREM-1, a novel receptor expressed on neutrophils and monocytes [J].
Bouchon, A ;
Dietrich, J ;
Colonna, M .
JOURNAL OF IMMUNOLOGY, 2000, 164 (10) :4991-4995
[2]   Monocyte functional responsiveness after PSGL-1-mediated platelet adhesion is dependent on platelet activation status [J].
Bournazos, Stylianos ;
Rennie, Jillian ;
Hart, Simon P. ;
Fox, Keith A. A. ;
Dransfield, Ian .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2008, 28 (08) :1491-1498
[3]   Antiplatelet Activity of Valproic Acid Contributes to Decreased Soluble CD40 Ligand Production in HIV Type 1-Infected Individuals [J].
Davidson, Donna C. ;
Hirschman, Michael P. ;
Spinelli, Sherry L. ;
Morrell, Craig N. ;
Schifitto, Giovanni ;
Phipps, Richard P. ;
Maggirwar, Sanjay B. .
JOURNAL OF IMMUNOLOGY, 2011, 186 (01) :584-591
[4]   Platelet-monocyte complex formation:: effect of blocking PSGL-1 alone, and in combination with αIIbβ3 and αMβ2, in coronary stenting [J].
Fernandes, LS ;
Conde, ID ;
Smith, CW ;
Kansas, GS ;
Snapp, KR ;
Bennet, N ;
Ballantyne, C ;
McIntire, LV ;
Smith, EO ;
Klem, JA ;
Mathew, S ;
Frangogiannis, N ;
Turner, NA ;
Maresh, KJ ;
Kleiman, NS .
THROMBOSIS RESEARCH, 2003, 111 (03) :171-177
[5]   CNS invasion by CD14+/CD16+peripheral blood-derived monocytes in HIV dementia:: perivascular accumulation and reservoir of HIV infection [J].
Fischer-Smith, T ;
Croul, S ;
Sverstiuk, AE ;
Capini, C ;
L'Heureux, D ;
Régulier, EG ;
Richardson, MW ;
Amini, S ;
Morgello, S ;
Khalili, K ;
Rappaport, J .
JOURNAL OF NEUROVIROLOGY, 2001, 7 (06) :528-541
[6]   Monocyte/macrophage trafficking in acquired immunodeficiency syndrome encephalitis: Lessons from human and nonhuman primate studies [J].
Fischer-Smith, Tracy ;
Bell, Christie ;
Croul, Sidney ;
Lewis, Mark ;
Rappaport, Jay .
JOURNAL OF NEUROVIROLOGY, 2008, 14 (04) :318-326
[7]   Platelet-monocyte aggregates - Bridging thrombosis and inflammation [J].
Freedman, JE ;
Loscalzo, J .
CIRCULATION, 2002, 105 (18) :2130-2132
[8]   PLATELET-ACTIVATING-FACTOR - A CANDIDATE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE 1-INDUCED NEUROTOXIN [J].
GELBARD, HA ;
NOTTET, HSLM ;
SWINDELLS, S ;
JETT, M ;
DZENKO, KA ;
GENIS, P ;
WHITE, R ;
WANG, L ;
CHOI, YB ;
ZHANG, DX ;
LIPTON, SA ;
TOURTELLOTTE, WW ;
EPSTEIN, LG ;
GENDELMAN, HE .
JOURNAL OF VIROLOGY, 1994, 68 (07) :4628-4635
[9]   Decreased platelet nitric oxide contributes to increased circulating monocyte-platelet aggregates in hypertension [J].
Gkaliagkousi, Eugenia ;
Corrigall, Valerie ;
Becker, Silke ;
de Winter, Patricia ;
Shah, Ashish ;
Zamboulis, Chrysanthos ;
Ritter, James ;
Ferro, Albert .
EUROPEAN HEART JOURNAL, 2009, 30 (24) :3048-3054
[10]   Increased circulating platelet-leucocyte complexes and platelet activation in patients with antiphospholipid syndrome, systemic lupus erythematosus and rheumatoid arthritis [J].
Joseph, JE ;
Harrison, P ;
Mackie, IJ ;
Isenberg, DA ;
Machin, SJ .
BRITISH JOURNAL OF HAEMATOLOGY, 2001, 115 (02) :451-459