Sepsis, complement and the dysregulated inflammatory response.

Sepsis, complement and the dysregulated inflammatory response.
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DOI:
10.1111/j.1582-4934.2009.00893.x
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发表时间:
2009-10
影响因子:
5.3
通讯作者:
Gao H
Gao H
中科院分区:
医学2区
文献类型:
--
作者:
Ward PA;Gao H

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Sepsis in human beings is a major problem involving many individuals and with a high death rate. Except for a single drug (recombinant activated protein C) that has been approved for treatment of septic patients, supportive measures represent the main clinical approach. There are many models of experimental sepsis, mostly in rodents. A commonly used model is cecal ligation and puncture (CLP). In this model, robust activation of complement occurs together with up-regulation of C5a receptors (C5aR, C5L2) in a variety of different organs (lungs, kidneys, liver, heart). In septic human beings there is abundant evidence for complement activation. Interception of C5a or its receptors in the CLP model greatly improves survival in septic rodents. There is compelling evidence that CLP causes an intense pro-inflammatory state and that C5a interaction with its receptors can be linked to apoptosis of the lymphoid system and cells of the adrenal medulla, loss of innate immune functions of blood neutrophils, consumptive coagulopathy and cardiac dysfunction. These findings may have implications for therapeutic interventions in human beings with sepsis.
补体过敏毒素C5A在实验性败血症过程中诱导肾上腺囊肿细胞的凋亡。
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