Bengtson Sara H, Phagoo Stephen B, Norrby-Teglund Anna, Påhlman Lisa, Mörgelin Matthias, Zuraw Bruce L, Leeb-Lundberg L M Fredrik, Herwald Heiko
Department of Clinical Sciences, Section for Clinical and Experimental Infection Medicine, Lund University, Tornavägen 10, SE-221 84 Lund, Sweden.
Blood. 2006 Sep 15;108(6):2055-63. doi: 10.1182/blood-2006-04-016444. Epub 2006 May 30.
An inappropriate host response to invading bacteria is a critical parameter that often aggravates the outcome of an infection. Staphylococcus aureus is a major human Gram-positive pathogen that causes a wide array of community- and hospital-acquired diseases ranging from superficial skin infections to severe conditions such as staphylococcal toxic shock. Here we find that S aureus induces inflammatory reactions by modulating the expression and response of the B1 and B2 receptors, respectively. This process is initiated by a chain of events, involving staphylococcal-induced cytokine release from monocytes, bacteria-triggered contact activation, and conversion of bradykinin to its metabolite desArg(9)bradykinin. The data of the present study implicate an important and previously unknown role for kinin receptor regulation in S aureus infections.
对入侵细菌的不适当宿主反应是一个关键参数，常常会加重感染的后果。金黄色葡萄球菌是一种主要的人类革兰氏阳性病原体，可引起从浅表皮肤感染到严重病症（如葡萄球菌中毒性休克）等一系列社区获得性和医院获得性疾病。我们在此发现，金黄色葡萄球菌分别通过调节B1和B2受体的表达及反应来诱导炎症反应。这一过程由一系列事件引发，包括葡萄球菌诱导单核细胞释放细胞因子、细菌触发的接触激活以及缓激肽向其代谢产物去精氨酸（9）缓激肽的转化。本研究的数据表明，激肽受体调节在金黄色葡萄球菌感染中具有重要且此前未知的作用。
