Expression of toll-like receptors on human platelets

被引:195
作者
Shiraki, R
Inoue, N
Kawasaki, S
Takei, A
Kadotani, M
Ohnishi, Y
Ejiri, J
Kobayashi, S
Hirata, K
Kawashima, S
Yokoyama, M
机构
[1] Kobe Univ, Grad Sch Med, Dept Internal Med, Div Cardiovasc & Resp Med, Kobe, Hyogo 6500017, Japan
[2] Kobe Steel Hosp, Dept Cardiovasc Med, Kakogawa, Japan
[3] Kobe Univ, Grad Sch Med, Dept Biol Informat, Div Surg Pathol, Kobe, Hyogo, Japan
关键词
coronary artery disease; infection; inflammation; thrombosis;
D O I
10.1016/j.thromres.2004.03.023
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Introduction: Platelets play a crucial role in arterial thrombosis, which is the main cause of acute coronary syndrome. Some mycobacteriums, such as Chlamydia pneumoniae, were associated with progression of atherosclerosis and they are interacted with Toll-like receptors (TLRs), which have been defined as pathogen-associated molecular pattern recognition molecules in innate immunity. In the present study, we examined whether human platelets express TLRs. Materials and methods: Human platelets were obtained from healthy volunteers and the mRNA and protein [eve( of TLRs on platelets and Meg-01 cells, megakaryoblastic cell line, were investigated. Results: Reverse transcription-polymerase chain reaction (RT-PCR) demonstrated that TLR1 and TLR6 mRNA were expressed in platelets and Meg-01 cells. Furthermore, interferon-gamma up-regulated their mRNA levels in dose and time dependent manners after stimuli. Both TLR1 and TLR6 proteins in platelets were detected by Western blotting, and their expression of platelets was more than that of Meg-01 cells. Flow cytometry analysis revealed the expression of TLR1 and TLR6 on the cell surface of Meg-01 cells. Furthermore, immunohistochemical analysis using human coronary thrombi obtained from patients with acute coronary syndrome confirmed the expression of TLR1 and TLR6 on platelets. Conclusion: In summary, we demonstrated that human platelets and Meg-01 cells expressed a family of TLRs for the first time, and our findings indicated that platelets might recognize antigens directly via TLRs. Our findings suggest a possibility that platelets have the ability to recognize the antigens via TLRs and that there are mechanistic relations between infectious inflammation and atherosclerotic vascular diseases. (C) 2004 Elsevier Ltd. All rights reserved.
引用
收藏
页码:379 / 385
页数:7
相关论文
共 15 条
[1]   Recognition of pathogen-associated molecular patterns by TLR family [J].
Akira, S ;
Hemmi, H .
IMMUNOLOGY LETTERS, 2003, 85 (02) :85-95
[2]   Toll-like receptors: critical proteins linking innate and acquired immunity [J].
Akira, S ;
Takeda, K ;
Kaisho, T .
NATURE IMMUNOLOGY, 2001, 2 (08) :675-680
[3]   Expression of toll-like receptors in human atherosclerotic lesions - A possible pathway for plaque activation [J].
Edfeldt, K ;
Swedenborg, J ;
Hansson, GK ;
Yan, ZQ .
CIRCULATION, 2002, 105 (10) :1158-1161
[4]  
Gupta S, 1997, J ALLERGY CLIN IMMUN, V99, P11
[5]   Cutting edge: Functional interactions between toll-like receptor (TLR) 2 and TLR1 or TLR6 in response to phenol-soluble modulin [J].
Hajjar, AM ;
O'Mahony, DS ;
Ozinsky, A ;
Underhill, DM ;
Aderem, A ;
Klebanoff, SJ ;
Wilson, CB .
JOURNAL OF IMMUNOLOGY, 2001, 166 (01) :15-19
[6]   Human platelets express heat shock protein receptors and regulate dendritic cell maturation [J].
Hilf, N ;
Singh-Jasuja, H ;
Schwarzmaier, P ;
Gouttefangeas, C ;
Rammensee, HG ;
Schild, H .
BLOOD, 2002, 99 (10) :3676-3682
[7]  
LEGRAND Y, 1978, THROMB HAEMOSTASIS, V39, P785
[8]   MOLECULAR-BASES OF THE ACUTE CORONARY SYNDROMES [J].
LIBBY, P .
CIRCULATION, 1995, 91 (11) :2844-2850
[9]   Influenza infection exerts prominent inflammatory and thrombotic effects on the atherosclerotic plaques of apolipoprotein E-deficient mice [J].
Naghavi, M ;
Wyde, P ;
Litovsky, S ;
Madjid, M ;
Akhtar, A ;
Naguib, S ;
Siadaty, MS ;
Sanati, S ;
Casscells, W .
CIRCULATION, 2003, 107 (05) :762-768
[10]   Chlamydia pneumoniae and chlamydial heat shock protein 60 stimulate proliferation of human vascular smooth muscle cells via Toll-like receptor 4 and p44/p42 mitogen-activated protein kinase activation [J].
Sasu, S ;
LaVerda, D ;
Qureshi, N ;
Golenbock, DT ;
Beasley, D .
CIRCULATION RESEARCH, 2001, 89 (03) :244-250