期刊
BLOOD
卷 108, 期 6, 页码 2055-2063出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2006-04-016444
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- NIAID NIH HHS [AI 50498] Funding Source: Medline
- NIGMS NIH HHS [GM 41659] Funding Source: Medline
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.
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