Flow cytometric study of in vitro neutrophil activation by biomaterials

被引:0
作者
Gorbet, MB
Yeo, EL
Sefton, MV [1 ]
机构
[1] Univ Toronto, Ctr Biomat, Dept Chem Engn & Appl Chem, Toronto, ON M5S 3E5, Canada
[2] Univ Toronto, Dept Math, Toronto, ON M5S 1A1, Canada
来源
JOURNAL OF BIOMEDICAL MATERIALS RESEARCH | 1999年 / 44卷 / 03期
关键词
flow cytometry; in vitro neutrophil activation; biomaterials;
D O I
10.1002/(SICI)1097-4636(19990305)44:3<289::AID-JBM7>3.0.CO;2-O
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
Neutrophil activation for adherent and nonadherent cells, as measured by flow cytometry, was not strongly dependent on material surface chemistry. We had hypothesized that material-induced neutrophil activation was an important parameter associated with material failure. All materials tested [cellophane, an acrylonitrile copolymer (AN69), Pellethane(TM) nylon, polyethylene terephthalate, low density polyethylene, and polydimethylsiloxane] activated isolated human neutrophils, which were resuspended in plasma or serum, to similar extents based on L-selectin shedding, CD11b upregulation, and stimulation of the oxidative burst after 30-min exposure. Inhibition of complement activation by sCR1 unexpectedly had Little effect if any on nonadherent neutrophils. However, neutrophil adhesion, but not the level of activation of the adherent cells, was strongly dependent on complement activation. Pretreatment with albumin did not inhibit adhesion or reduce neutrophil activation, but plasma pretreatment resulted in increased activation for nonadherent and adherent cells. More adhesion and a higher level of activation of adherent cells was observed following pretreatment with fibrinogen, a ligand of CD11b. Taken together these results suggest that upon contact with a material, neutrophil activation may occur though mechanisms that are not mediated by complement. For example, the presence of plasma proteins such as fibrinogen at the interface may trigger activation and the release of other activating agents. Although the material differences are small, the extent of activation may be significant and warrant further study of the mechanism and consequences of that activation. (C) 1999 John Wiley & Sons, Inc.
引用
收藏
页码:289 / 297
页数:9
相关论文
共 33 条
[1]  
AMAOUT MA, 1990, BLOOD, V75, P1037
[2]  
Amiji MM, 1995, POLYM BIOMATERIALS S, P535
[3]   USING ELISA TO EVALUATE COMPLEMENT ACTIVATION BY REFERENCE BIOMATERIALS [J].
BERGER, M ;
BROXUP, B ;
SEFTON, MV .
JOURNAL OF MATERIALS SCIENCE-MATERIALS IN MEDICINE, 1994, 5 (9-10) :622-627
[4]  
BLEEKER WK, 1985, BACTERIAL ENDOTOXINS, P293
[5]  
BOHLER J, 1993, NEPHROL DIAL TRANSPL, V8, P1359
[6]  
Casimir CM, 1994, IMMUNOPHARMACOLOGY N, P27
[7]   ANALYSIS OF THE COMPLEMENT C-3 FRAGMENTS ASSOCIATED WITH HEMODIALYSIS MEMBRANES [J].
CHEUNG, AK ;
PARKER, CJ ;
JANATOVA, J .
KIDNEY INTERNATIONAL, 1989, 35 (02) :576-588
[8]   ADSORPTION OF UNACTIVATED COMPLEMENT PROTEINS BY HEMODIALYSIS MEMBRANES [J].
CHEUNG, AK .
AMERICAN JOURNAL OF KIDNEY DISEASES, 1989, 14 (06) :472-477
[9]   ADHERENCE OF NEUTROPHILS TO HEMODIALYSIS MEMBRANES - ROLE OF COMPLEMENT RECEPTORS [J].
CHEUNG, AK ;
HOHNHOLT, M ;
GILSON, J .
KIDNEY INTERNATIONAL, 1991, 40 (06) :1123-1133
[10]  
CRISTOL JP, 1994, NEPHROL DIAL TRANSPL, V9, P389