White cell apoptosis in platelet concentrates

被引:19
作者
Frabetti, F
Tazzari, PL
Musiani, D
Bontadini, A
Matteini, C
Roseti, L
Tassi, C
Viggiani, M
Marini, M
Conte, R
机构
[1] Policlin S Orsola, Immunohematol & Transfus Serv, Bologna, Italy
[2] Univ Bologna, Inst Histol & Gen Embryol, Bologna, Italy
关键词
D O I
10.1046/j.1537-2995.2000.40020160.x
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
BACKGROUND: The aim of the present study was the evaluation of the apoptosis in residual white cells (WBCs) contained in platelet concentrates (PCs) and of the relationship of this apoptosis with the concentration of inflammatory cytokines in the medium and with platelet activation. STUDY DESIGN AND METHODS: Three independent methods were used to evaluated apoptosis in WBCs present in 9 PCs, either from single donors by apheresis (SD-PCs) or from pooled buffy coats (BC-PCs). All PCs were divided in two parts, one of which was irradiated. PCs were stored up to 4 days at room temperature, and samples were withdrawn daily for analysis of apoptosis, of platelet activation (surface and soluble CD62P), and of cytokine concentration (interleukin [IL]-1 alpha, IL-1 beta, IL-6, IL-8, and tumor necrosis factor alpha). RESULTS: Apoptosis was found to occur with storage in both irradiated and nonirradiated units. Platelet activation increased with storage time and was higher in BC-PCs. The amount of released cytokines was rather variable among PC units. Only IL-8 was consistently found to increase with storage time. CONCLUSIONS: Apoptosis of residual WBCs occurred in PC units as a function of storage time. The amount and the timecourse of apoptosis seem to correlate with IL-8 release rather than with platelet activation or with the occurrence of febrile nonhemolytic transfusion reactions.
引用
收藏
页码:160 / 168
页数:9
相关论文
共 39 条
[1]
Interaction with autologous platelets multiplies interleukin-1 and tumor necrosis factor production in mononuclear cells [J].
Aiura, K ;
Clark, BD ;
Dinarello, CA ;
Margolis, NH ;
Kaplanski, G ;
Burke, JF ;
Tompkins, RG ;
Gelfand, JA .
JOURNAL OF INFECTIOUS DISEASES, 1997, 175 (01) :123-129
[2]
Morphological and biochemical characterization and analysis of apoptosis [J].
Allen, RT ;
Hunter, WJ ;
Agrawal, DK .
JOURNAL OF PHARMACOLOGICAL AND TOXICOLOGICAL METHODS, 1997, 37 (04) :215-228
[3]
Andonegui G, 1997, J IMMUNOL, V158, P3372
[4]
Hypothesis: Is soluble P-selectin a new marker of platelet activation? [J].
Blann, AD ;
Lip, GYH .
ATHEROSCLEROSIS, 1997, 128 (02) :135-138
[5]
Bolognesi A, 1996, INT J CANCER, V68, P349, DOI 10.1002/(SICI)1097-0215(19961104)68:3<349::AID-IJC13>3.0.CO
[6]
2-3
[7]
COHEN JJ, 1993, IMMUNOL TODAY, V14, P126, DOI 10.1016/0167-5699(93)90214-6
[8]
White cell apoptosis in packed red cells [J].
Frabetti, F ;
Musiani, D ;
Marini, M ;
Fanelli, C ;
Coppola, S ;
Ghibelli, L ;
Tazzari, PL ;
Bontadini, A ;
Tassi, C ;
Conte, R .
TRANSFUSION, 1998, 38 (11-12) :1082-1089
[9]
The diadenosine polyphosphates Ap(3)A and Ap(4)A and adenosine triphosphate interact with granulocyte-macrophage colony-stimulating factor to delay neutrophil apoptosis: Implications for neutrophil platelet interactions during inflammation [J].
Gasmi, L ;
McLennan, AG ;
Edwards, SW .
BLOOD, 1996, 87 (08) :3442-3449
[10]
Apoptosis of vascular smooth muscle cells induced by in vitro stimulation with interferon-gamma, tumor necrosis factor-alpha, and interleukin-1 beta [J].
Geng, YJ ;
Wu, Q ;
Muszynski, M ;
Hansson, GK ;
Libby, P .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1996, 16 (01) :19-27