Dacron vascular biomaterial triggers macrophage ectoenzyme activity without change in cell membrane fluidity
- 1 August 1993
- journal article
- research article
- Published by Wiley in Journal of Biomedical Materials Research
- Vol. 27 (8) , 1087-1094
- https://doi.org/10.1002/jbm.820270814
Abstract
Biomaterials induce an inflammatory reaction characterized by a rapid recruitment at the implantation site of polymorphonuclear cells and macrophages. In the course of the inflammatory response, the cellular activation triggers expression of a number of enzymes, such as 5′‐nucleotidase, which is widely distributed in animal cell membranes as an ectoenzyme. It is now well established that 5′‐nucleotidase activity decreses following the contact of inflammatory cells with foreign particles. In this paper we investigate a possible correlation between the enzymatic activities and the dynamic properties of the cell membrane bilayer. Dacron pieces were introduced into rats' peritoneal cavities for a period of 6 h, after which the peritoneal cells were harvested, and various enzyme assays performed, including those for cytoplasmic, lysosomal, and ectoenzymes. In parallel, we studied cell membrane fluidity, using fluorescence polarization of 1‐(4‐trimethylammoniumphenyl)‐6‐phenyl‐1,3,5‐hexatriene (TMA‐DPH), and cellular ultrastructural alteration resulting from the cell‐biomaterial interactions using scanning and transmission electron microscopy. Our results show that: (1) macrophages spread around the Dacron fibers with cytoplasmic finger‐like projections, but no phagolysosomes, (2) 5′‐nucleotidase levels decrease with surgical trauma in comparison with the resident cell exudate, (3) implantation of biomaterials slightly modify the 5′‐nucleotidase levels observed in the sham animal, (4) no differences in the anisotropy values indicating that membrane lipid order within the cells could not account for the observed decrease of 5′‐nucleotidase activity. Thus, we can suggest that 5′‐nucleotidase expression may reflect a particular feature of cell activation without a phagocytic process. © 1993 John Wiley & Sons, Inc.Keywords
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