Platelet-leukocyte activation during hemodialysis detected with a monoclonal antibody to leukocyte integrin CD11b

被引:24
作者
Hernández, MR
Galán, AM
Lozano, M
Bozzo, J
Cases, A
Escolar, G
Calls, J
Ordinas, A
机构
[1] Hosp Clin Barcelona, Serv Hemoterapia & Hemostasia, E-08036 Barcelona, Spain
[2] Hosp Clin Barcelona, Serv Nefrol, E-08036 Barcelona, Spain
关键词
hemodialysis; CD11b; cross-talk; heterotypic aggregates;
D O I
10.1159/000045167
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Platelet activation is commonly monitored with a battery of monoclonal antibodies against different platelet epitopes with controversial results. The transient expression of platelet markers and their role mediating interactions with other cells could easily explain these discrepancies. The present study has evaluated whether the analysis of a leukocyte activation antigen (CD11b) could provide more reliable results than detection of platelet activation markers. Cytometric techniques with specific monoclonal antibodies were used to compare the reliability of platelet and leukocyte markers to detect activation. Modifications in the presence of platelet glycoproteins GPIb (CD42b), GPIIIa (CD41) and GPIV (CD36), expression of specific platelet markers (P-selectin (CD62P) and lysosomal protein (CD63)) and leukocyte integrin (CD11b) were assessed during hemodialysis. Platelet antigens remained in uremic patients at levels similar or slightly above those detected in a group of healthy subjects. Modifications of platelet antigens during hemodialysis produced inconclusive results. However, numbers of leukocytes expressing CD11b increased progressively during hemodialysis (17.2 +/- 5.1% at 15 min and 21.3 +/-. 6.6% at 2 h, p < 0.05, vs. baseline 6.9 +/- 0.2%). The hemodialysis procedure caused an increased formation of leukocyte-platelet aggregates. Detection of leukocyte CD11b may be a useful marker of overall cellular activation during the hemodialysis procedure.
引用
收藏
页码:197 / 203
页数:7
相关论文
共 41 条
[1]   ADHESION MOLECULES AND INFLAMMATORY INJURY [J].
ALBELDA, SM ;
SMITH, CW ;
WARD, PA .
FASEB JOURNAL, 1994, 8 (08) :504-512
[2]   INCREASED EXPRESSION OF AN ADHESION-PROMOTING SURFACE GLYCOPROTEIN IN THE GRANULOCYTOPENIA OF HEMODIALYSIS [J].
ARNAOUT, MA ;
HAKIM, RM ;
TODD, RF ;
DANA, N ;
COLTEN, HR .
NEW ENGLAND JOURNAL OF MEDICINE, 1985, 312 (08) :457-462
[3]   LEUKOCYTE ADHESION MOLECULES DEFICIENCY - ITS STRUCTURAL BASIS, PATHOPHYSIOLOGY AND IMPLICATIONS FOR MODULATING THE INFLAMMATORY RESPONSE [J].
ARNAOUT, MA .
IMMUNOLOGICAL REVIEWS, 1990, 114 :145-180
[4]   The molecular mechanism of platelet adhesion [J].
Berndt, MC ;
Ward, CM ;
DeLuca, M ;
Facey, DA ;
Castaldi, PA ;
Harris, SJ ;
Andrews, RK .
AUSTRALIAN AND NEW ZEALAND JOURNAL OF MEDICINE, 1995, 25 (06) :822-830
[5]   COMPLEMENT ACTIVATION DURING EXTRACORPOREAL-CIRCULATION [J].
BILFINGER, TV .
ADVANCES IN NEUROIMMUNOLOGY, 1993, 3 (04) :269-276
[6]   Hypothesis: Is soluble P-selectin a new marker of platelet activation? [J].
Blann, AD ;
Lip, GYH .
ATHEROSCLEROSIS, 1997, 128 (02) :135-138
[7]  
BUTTRUM SM, 1993, BLOOD, V82, P1165
[8]   BETA-2 INTEGRINS ARE REQUIRED FOR NEUTROPHIL DEGRANULATION INDUCED BY HEMODIALYSIS MEMBRANES [J].
CHEUNG, AK ;
PARKER, CJ ;
HOHNHOLT, M .
KIDNEY INTERNATIONAL, 1993, 43 (03) :649-660
[9]   COOPERATION BETWEEN PLATELETS AND NEUTROPHILS FOR PAF-ACETHER (PLATELET-ACTIVATING FACTOR) FORMATION [J].
COEFFIER, E ;
DELAUTIER, D ;
LECOUEDIC, JP ;
CHIGNARD, M ;
DENIZOT, Y ;
BENVENISTE, J .
JOURNAL OF LEUKOCYTE BIOLOGY, 1990, 47 (03) :234-243
[10]   HEMODIALYSIS LEUKOPENIA - PULMONARY VASCULAR LEUKOSTASIS RESULTING FROM COMPLEMENT ACTIVATION BY DIALYZER CELLOPHANE MEMBRANES [J].
CRADDOCK, PR ;
FEHR, J ;
DALMASSO, AP ;
BRIGHAM, KL ;
JACOB, HS .
JOURNAL OF CLINICAL INVESTIGATION, 1977, 59 (05) :879-888