Mannose-binding lectin and its associated proteases (MASPs) mediate coagulation and its deficiency is a risk factor in developing complications from infection, including disseminated intravascular coagulation
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- 作者：Kazue Takahashi ; Wei-Chuan Chang ; Minoru Takahashi ; Vasile Pavlov ; Yumi Ishida ; Laura La Bonte ; Lei Shi ; Teizo Fujita ; Gregory L. Stahl ; Elizabeth M. Van Cott
- 关键词：Mannose-binding lectin ; MASP ; Deficiency ; Infection ; Coagulation ; Inflammation
- 刊名：Immunobiology
- 出版年：2011
- 出版时间：January-February 2011
- 年：2011
- 卷：216
- 期：1-2
- 页码：96-102
- 全文大小：403 K
文摘
The first line of host defense is the innate immune system that includes coagulation factors and pattern recognition molecules, one of which is mannose-binding lectin (MBL). Previous studies have demonstrated that MBL deficiency increases susceptibility to infection. Several mechanisms are associated with increased susceptibility to infection, including reduced opsonophagocytic killing and reduced lectin complement pathway activation. In this study, we demonstrate that MBL and MBL-associated serine protease (MASP)-1/3 together mediate coagulation factor-like activities, including thrombin-like activity. MBL and/or MASP-1/3 deficient hosts demonstrate in vivo evidence that MBL and MASP-1/3 are involved with hemostasis following injury. Staphylococcus aureus infected MBL null mice developed disseminated intravascular coagulation (DIC), which was associated with elevated blood IL-6 levels (but not TNF-α and multi-organ inflammatory responses). Infected MBL null mice also develop liver injury. These findings suggest that MBL deficiency may manifest into DIC and organ failure during infectious diseases.