Biofilms and Inflammation in Chronic Wounds

被引:304
|
作者
Zhao, Ge [1 ]
Usui, Marcia L. [1 ]
Lippman, Soyeon I. [2 ]
James, Garth A. [3 ]
Stewart, Philip S. [3 ]
Fleckman, Philip [1 ]
Olerud, John E. [1 ]
机构
[1] Univ Washington, Div Dermatol, Box 356524, Seattle, WA 98195 USA
[2] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA
[3] Montana State Univ, Ctr Biofilm Engn, Bozeman, MT 59717 USA
关键词
D O I
10.1089/wound.2012.0381
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Significance: The incidence, cost, morbidity, and mortality associated with non-healing of chronic skin wounds are dramatic. With the increasing numbers of people with obesity, chronic medical conditions, and an increasing life expectancy, the healthcare cost of non-healing ulcers has recently been estimated at $25 billion annually in the United States. The role played by bacterial biofilm in chronic wounds has been emphasized in recent years, particularly in the context of the prolongation of the inflammatory phase of repair. Recent Advances: Rapid high-throughput genomic approaches have revolutionized the ability to identify and quantify microbial organisms from wounds. Defining bacterial genomes and using genetic approaches to knock out specific bacterial functions, then studying bacterial survival on cutaneous wounds is a promising strategy for understanding which genes are essential for pathogenicity. Critical Issues: When an animal sustains a cutaneous wound, understanding mechanisms involved in adaptations by bacteria and adaptations by the host in the struggle for survival is central to development of interventions that favor the host. Future Directions: Characterization of microbiomes of clinically well characterized chronic human wounds is now under way. The use of in vivo models of biofilm-infected cutaneous wounds will permit the study of the mechanisms needed for biofilm formation, persistence, and potential synergistic interactions among bacteria. A more complete understanding of bacterial survival mechanisms and how microbes influence host repair mechanisms are likely to provide targets for chronic wound therapy.
引用
收藏
页码:389 / 399
页数:11
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