Activation and control of complement, inflammation, and infection associated with the use of biomedical polymers

被引:42
作者
Janatova, J
机构
[1] Univ Utah, Dept Bioengn, Salt Lake City, UT 84112 USA
[2] Univ Utah, Ctr Biopolymers Interfaces, Salt Lake City, UT 84112 USA
关键词
D O I
10.1097/00002480-200011000-00038
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
It is generally acknowledged that artificial biomaterials are much less immunologically active than transplants or tissue derived biomaterials. However, activation of both the coagulation cascade and the complement system is a common occurrence when human blood is exposed to biomaterial surfaces during extracorporeal procedures, such as renal hemodialysis or cardiopulmonary bypass. Both individual and collective activation of these cascades often produce local and systemic effects. A number of complement activation products function as the mediators of inflammation. They serve as ligands for specific receptors on polymorphonuclear leukocytes, monocytes, macrophages, mast cells, and other cells. Such an interaction leads to induction of cellular responses in adhered cells, including release of oxidative products, lysosomal enzymes, or both, which often contribute to a number of pathologic conditions. Most pathogens invading the human body are attacked by the immune system directly following entry, especially when they are in contact with blood. However, bacteria and parasites have developed a large number of specific strategies to overcome immune defense among others by avoiding either recognition or eradication by complement. In this aspect, of concern are several microorganisms responsible for formation of antibiotic resistant biofilms on biomaterial surfaces, namely Staphylococcus epidermidis, Staphylococcus aureus, and Pseudomonas aeruginosa.
引用
收藏
页码:S53 / S62
页数:10
相关论文
共 102 条
[1]  
ANWAR H, 1992, FEMS MICROBIOL LETT, V92, P235, DOI 10.1111/j.1574-6968.1992.tb05267.x
[2]  
BOHLER J, 1993, NEPHROL DIAL TRANSPL, V8, P1359
[3]  
BROWN EJ, 1985, CURR TOP MICROBIOL, V121, P159
[4]   COMPLEMENT ACTIVATION IN EXTRACORPOREAL CIRCUITS [J].
CHENOWETH, DE .
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, 1987, 516 :306-313
[5]   DEMONSTRATION OF SPECIFIC C5A RECEPTOR ON INTACT HUMAN POLYMORPHONUCLEAR LEUKOCYTES [J].
CHENOWETH, DE ;
HUGLI, TE .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1978, 75 (08) :3943-3947
[6]   ACTIVATION OF COMPLEMENT BY HEMODIALYSIS MEMBRANES - POLYACRYLONITRILE BINDS MORE C3A THAN CUPROPHAN [J].
CHEUNG, AK ;
PARKER, CJ ;
WILCOX, LA ;
JANATOVA, J .
KIDNEY INTERNATIONAL, 1990, 37 (04) :1055-1059
[7]  
CHEUNG AK, 1992, J AM SOC NEPHROL, V2, P1328
[8]  
CHEUNG AK, 1990, J AM SOC NEPHROL, V1, P150
[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]  
CHOI NH, 1989, MOL IMMUNOL, V26, P835