Current status of pathogenetic mechanisms in staphylococcal arthritis
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- 作者：Tarkowski ; Andrej ; Bokarewa ; Maria ; Collins ; L. Vincent ; Gjertsson ; Inger ; Hultgren ; Olof H. ; et. al.
- 关键词：Staphylococcal arthritis ; Pathogenetic mechanism ; Host-bacterium interaction
- 刊名：FEMS Microbiology Letters
- 出版年：2002
- 出版时间：December 17, 2002
- 年：2002
- 卷：217
- 期：2
- 页码：125-132
- 全文大小：225 K
文摘
Interactions between staphylococci and the joint tissues of the host lead typically to rapidly progressing and highly destructive processes. Staphylococci possess a vast arsenal of components and products that contribute to the pathogenesis of joint infection. Occasionally these compounds have overlapping activities and act either in concert or alone. Host responsiveness to staphylococcal infection displays an even more complex pattern. Most of the cells and molecules that participate in the innate immune system protect the host against bacteria. However, the staphylococci have developed systems that counteract endogenous protective mechanisms. Interestingly, certain cells and molecules of the acquired immune system potentiate the severity of infection by triggering exaggerated responses to the staphylococcal danger signals. This review deals with the intricate host–bacterium interactions that occur during experimental septic arthritis, and outlines potential preventive and treatment modalities.