金黄色葡萄球菌感染期间激肽受体的表达
Kinin receptor expression during Staphylococcus aureus infection.
作者信息
Bengtson Sara H, Phagoo Stephen B, Norrby-Teglund Anna, Påhlman Lisa, Mörgelin Matthias, Zuraw Bruce L, Leeb-Lundberg L M Fredrik, Herwald Heiko
机构信息
Department of Clinical Sciences, Section for Clinical and Experimental Infection Medicine, Lund University, Tornavägen 10, SE-221 84 Lund, Sweden.
出版信息
Blood. 2006 Sep 15;108(6):2055-63. doi: 10.1182/blood-2006-04-016444. Epub 2006 May 30.
Abstract
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.
摘要
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。
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本文引用的文献
1
The role of CD1d-restricted NK T lymphocytes in the immune response to oral infection with Salmonella typhimurium.CD1d 限制性自然杀伤 T 淋巴细胞在对鼠伤寒沙门氏菌口腔感染的免疫反应中的作用。
Eur J Immunol. 2005 Jul;35(7):2100-9. doi: 10.1002/eji.200425846.
2
International union of pharmacology. XLV. Classification of the kinin receptor family: from molecular mechanisms to pathophysiological consequences.国际药理学联合会。XLV。激肽受体家族的分类：从分子机制到病理生理后果。
Pharmacol Rev. 2005 Mar;57(1):27-77. doi: 10.1124/pr.57.1.2.
3
Interplay between superantigens and immunoreceptors.超抗原与免疫受体之间的相互作用。
Scand J Immunol. 2004 Apr;59(4):345-55. doi: 10.1111/j.0300-9475.2004.01404.x.
4
M protein, a classical bacterial virulence determinant, forms complexes with fibrinogen that induce vascular leakage.M蛋白是一种典型的细菌毒力决定因素，它与纤维蛋白原形成复合物，从而导致血管渗漏。
Cell. 2004 Feb 6;116(3):367-79. doi: 10.1016/s0092-8674(04)00057-1.
5
Role of inflammatory mediators in the pathophysiology of acute respiratory distress syndrome.炎症介质在急性呼吸窘迫综合征病理生理学中的作用
J Pathol. 2004 Feb;202(2):145-56. doi: 10.1002/path.1491.
6
Quorum sensing in Staphylococcus infections.葡萄球菌感染中的群体感应
J Clin Invest. 2003 Dec;112(11):1620-5. doi: 10.1172/JCI20442.
7
Requirement for direct cross-talk between B1 and B2 kinin receptors for the proliferation of androgen-insensitive prostate cancer PC3 cells.雄激素不敏感前列腺癌PC3细胞增殖中B1和B2激肽受体之间直接相互作用的必要性。
Biochem J. 2003 Apr 15;371(Pt 2):581-7. doi: 10.1042/BJ20021708.
8
Points of control in inflammation.炎症中的控制点。
Nature. 2002;420(6917):846-52. doi: 10.1038/nature01320.
9
Human B1 and B2 bradykinin receptors and their agonists target caveolae-related lipid rafts to different degrees in HEK293 cells.人类B1和B2缓激肽受体及其激动剂在HEK293细胞中对小窝相关脂筏的靶向程度不同。
Biochemistry. 2002 Dec 3;41(48):14340-7. doi: 10.1021/bi020231d.
10
Functional expression of the C-X-C chemokine receptor CXCR4 by human bronchial epithelial cells: regulation by proinflammatory mediators.人支气管上皮细胞C-X-C趋化因子受体CXCR4的功能性表达：促炎介质的调节作用
J Immunol. 2002 Dec 1;169(11):6445-51. doi: 10.4049/jimmunol.169.11.6445.
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