Increased expression of Toll like receptor 4 on peripheral-blood mononuclear cells in patients with coronary arteriosclerosis disease

被引:47
作者
Geng, HL [1 ]
Lu, HQ [1 ]
Zhang, LZ [1 ]
Zhang, H [1 ]
Zhou, L [1 ]
Wang, H [1 ]
Zhong, RQ [1 ]
机构
[1] Second Mil Med Univ, Changzheng Hosp, Dept Lab Diagnosis, Shanghai, Peoples R China
关键词
toll-like receptor 4; atherosclerosis; lipid; inflammation;
D O I
10.1111/j.1365-2249.2005.02982.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
摘要
The family of Toll-like receptors (TLRs) initiates innate immune responses, and Toll-like receptor 4 (TLR4) was considered to be an important player in the initiation and progression of atherosclerotic disease. The aim of the study was to investigate the expression of TLR4 on peripheral-blood mononuclear cells (PBMCs) in patients with coronary arteriosclerosis disease (CAD). We have examined the expression of TLR4 protein and mRNA by flow cytometry (FCM) and real-time quantitative reverse transcription polymerase chain reaction (RT-PCR). In addition, the levels of plasma lipids were determined by automatic biochemistry analyzer. The results showed that the positive rates and the mean mRNA copy number of TLR4 in CAD group were significantly higher than that in controls. But no significant difference was found in the positive rate and the mean mRNA copy number of TLR4 between CAD group with normal level of plasma lipids and the CAD group with abnormal level of plasma lipids. We suggest that expression level of TLR4 on peripheral-blood mononuclear cells is increased in atherosclerotic, but the differential expression of TLR4 has no correlation with the level of plasma lipids.
引用
收藏
页码:269 / 273
页数:5
相关论文
共 22 条
[11]
Hoshino K, 1999, J IMMUNOL, V162, P3749
[12]
Toll-like receptor 4 polymorphisms and atherogenesis [J].
Kiechl, S ;
Lorenz, E ;
Reindl, M ;
Wiedermann, CJ ;
Oberhollenzer, F ;
Bonora, E ;
Willeit, J ;
Schwartz, DA .
NEW ENGLAND JOURNAL OF MEDICINE, 2002, 347 (03) :185-192
[13]
Toll-like receptor 4 and atherogenesis [J].
Kiechl, S ;
Wiedermann, CJ ;
Willeit, J .
ANNALS OF MEDICINE, 2003, 35 (03) :164-171
[14]
A human homologue of the Drosophila Toll protein signals activation of adaptive immunity [J].
Medzhitov, R ;
PrestonHurlburt, P ;
Janeway, CA .
NATURE, 1997, 388 (6640) :394-397
[15]
TLR signaling: An emerging bridge from innate immunity to atherogenesis [J].
Michelsen, KS ;
Doherty, TM ;
Shah, PK ;
Arditi, M .
JOURNAL OF IMMUNOLOGY, 2004, 173 (10) :5901-5907
[16]
Minimally modified LDL binds to CD14, induces macrophage spreading via TLR4/MD-2, and inhibits phagocytosis of apoptotic cells [J].
Miller, YI ;
Viriyakosol, S ;
Binder, CJ ;
Feramisco, JR ;
Kirkland, TN ;
Witztum, JL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (03) :1561-1568
[17]
Role of Toll-like receptor 4 in the initiation and progression of atherosclerotic disease [J].
Pasterkamp, G ;
van Keulen, JK ;
de Kleijn, DPV .
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, 2004, 34 (05) :328-334
[18]
Endotoxin-tolerant mice have mutations in toll-like receptor 4 (Tlr4) [J].
Qureshi, ST ;
Larivière, L ;
Leveque, G ;
Clermont, S ;
Moore, KJ ;
Gros, P ;
Malo, D .
JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 189 (04) :615-625
[19]
Mechanisms of disease - Atherosclerosis - An inflammatory disease [J].
Ross, R .
NEW ENGLAND JOURNAL OF MEDICINE, 1999, 340 (02) :115-126
[20]
Shah Prediman K., 1999, Cardiology Clinics, V17, P271, DOI 10.1016/S0733-8651(05)70074-6